Gout (excluding septic arthritis)


  • Diagnosis and management of gout and pseudogout, in adults within primary care.

Out of scope

  • Diagnosis and management of septic arthritis.


Signs and Symptoms

Gout caused by urate crystals and can occur as acute attack or recurrent attack

Gout usually causes a monoarthritis with pain that is extremely severe "the worst pain I've ever had – 11/10 severity"

Pain often maximizes in first 6-12 hours and resolves in 3-10 days

Usually a monoarthritis which is hot, red, swollen and extremely tender – often 1st MTP joint but can affect any small or large joint

Gout is usually a clinical diagnosis

Associations with metabolic syndrome and increased risk of cardiovascular disease

History and Examination

Age - onset in:

  • someone less than age 30 years may suggest:
    • a genetic cause, renal disease, enzymatic disorder
  • the elderly - disease more likely to be:
    • polyarticular, involving the upper limb, associated with tophi

Ask about the pain:

  • location - commonly the first metatarsophalangeal joint, but can also affect joints in the:
    • foot, ankle, knee, wrist, finger - particularly associated with diuretic -induced gout, elbow
  • timing:
    • an acute attack of gout typically occurs during the night
    • pain usually reaches its worst within 6-12 hours - although it has been noted that pain can take as long as 24 hours to reach its maximum intensity
    • pain usually resolves within 3-10 days
  • precipitating events including:
    • intercurrent illness,
    • surgery
    • dehydration, e.g. going on holiday to a country with a hot climate or alcohol excess
  • if there has been any resolution of symptoms - acute gout can resolve spontaneously without treatment within 7-10 days, after which a patient can be symptom-free for months or years

Accompanying symptoms may occur, such as:

  • low-grade fever, general malaise, anorexia

Determine the presence of risk factors which include:

  • increasing age
  • non-white ethnicity
  • obesity - especially central obesity
  • family history
  • diet - specifically consumption of:
    • meat, fish, dietary fructose
  • alcohol consumption - particularly beer

Certain medications:

  • diuretics- particularly loop and thiazide diuretics, low dose aspirin and salicylates, antileukemic agents, cyclosporine, adrenaline, ergotamine, ethacrynic acid, ethanol , nicotinic acid, pyrazinamide, cytotoxic drugs, ethambutol, tacrolimus, lead exposure

Associated co-morbidities:

  • insulin resistance, dyslipidaemia, hypertension cardiovascular disorder, renal impairment, diabetes, myeloproliferative disease, severe psoriasis

Examine affected joint(s) for the following features:

  • erythema, warm temperature, swelling, tenderness, reduced range of movement

NB: The extent of the inflammatory response in crystal arthropathy is usually extreme and profound erythema and exquisite tenderness,e.g. inability to tolerate bed clothes on joint, are almost diagnostic features.

For patients with recurrent or chronic gout, examine for tophi:

  • deposits of urate embedded in a matrix of lipid protein and calcific debris
    • usually found subcutaneously in the: hands, feet, elbows, ears, olecranon bursae
  • can also occur in the eye, bone

NB: Inflammation can also affect tendons and soft tissue causing diffuse oedema and cellulitis - this often causes diagnostic confusion and inappropriate antibiotic therapy.

Regarding pseudogout:

  • examine for:
    • tenderness in commonly affected joints: knee, shoulder, elbow, wrist
  • signs of severe accelerated osteoarthritis with bony hypertrophic changes
  • other suggestive changes:
    • chondrocalcinosis
    • severe joint damage - much more than would be seen in simple osteoarthritis, e.g. very asymmetrical disease

Differential Diagnoses

Seek specialist advice when:

  • The diagnosis is uncertain, there is a suspicion of an underlying systemic illness (e.g. rheumatoid arthritis or connective tissue disorder), or gout occurs during pregnancy or in a young person (under 25 years of age).
  • Allopurinol or febuxostat is at maximum dose but a person is still having recurrent attacks of gout.
  • A person has persistent symptoms during an acute attack despite maximum doses of anti-inflammatory medication (alone or in combination).
  • An intra-articular steroid injection is indicated but the facilities or expertise are not available.
  • Complications are present, including urate kidney stones, urate nephropathy, or troublesome tophi.

Red Flags

Alarm features of septic arthritis - how to tell?
  • gout usually presents in the metatarsophalangeal (MTP) joint – if first episode not in MTP joint then joint needs aspirating
  • systemic features of sepsis
  • septic joints get worse rather than better
  • prostheses in-situ
  • gout is very rare in premenopausal women or men under 30 years of age

Please refer suspected septic joints to the on-call orthopaedic team for joint aspiration.

  • Is not diagnostic and may be falsely normal in an acute attack
  • The main use of urate is in titrating prophylactic treatments e.g. allopurinol


Although the diagnosis of acute gout is usually made clinically, all patients with a suspected first attack should be investigated to:

  • obtain evidence to support the diagnosis
  • look for underlying causes
  • identify associated co-morbidities

NB: If septic arthritis is a differential, make sure to perform blood cultures.

Consider the following investigations for the causes of gout:
  • full blood count (FBC):
    • may reveal: myelo and lymphoproliferative disorders, secondary polycythaemia, haemolytic anaemia, haemoglobinopathies
    • white cell count may be slightly raised with gout - if it is very high consider septic arthritis
  • liver enzymes may reveal:
    • alcohol abuse
    • impaired renal function - if detected, medication doses may need adjusting
  • investigations for the inherited metabolic disorders:
    • should be reserved for those with a relevant family history
      • examples include: Lesch-Nyhan syndrome, glucose - 6-phosphate dehydrogenase deficiency

Regarding investigations for the diagnosis of gout: the American College of Rheumatology (ACR) criteria for diagnosing gout is as follows:

  • characteristic urate crystals in joint fluid; or
  • a tophus proved to contain urate crystals
  • the presence of six or more defined laboratory and x-ray phenomena
Serum urate:
  • be aware that serum urate is not essential for a diagnosis as it may fall during an acute attack - only to rise a few weeks later
  • should be measured in patients with a history of renal colic- one in five patients with gout over-excrete urate which leads to the formation of urate stones
Joint aspiration:
  • can demonstrate urate crystals in the synovial fluid
  • usually reserved for when the diagnosis is uncertain, as even though it is considered the gold standard for confirming gout, aspirating an acutely inflamed joint is unnecessary when the diagnosis can be made clinically
Consider the following investigations for the diagnosis of chronic or recurrent gout:
  • tophi aspiration - can demonstrate urate crystals in aspirate
  • X-ray
    • tophi can be seen as soft tissue swellings, occasionally associated with calcifications
    • useful in chronic gout to distinguish between osteoarthritis and rheumatoid arthritis changes
    • destructive changes may be an indication for urate lowering therapy
    • demonstrates characteristic changes including the presence of:
      • subcortical cysts without erosions
      • geodes - punched-out type erosions with sclerotic margins and overhanging edges
Screen for co-morbidities associated with gout using the following investigations:
  • blood pressure, cholesterol, blood sugar, thyroid function (TFTs), uric acid secretion - consider if:
  • strong family history of gout; or onset of gout is under age 25 years; or renal stones are present
Consider the following investigations to screen for conditions associated with pseudogout:
  • calcium, magnesium, ferritin, TFTs
Consider the following investigations for the diagnosis of pseudogout:
  • joint or tophi aspiration - demonstrates pyrophosphate crystals in the synovial fluid
  • X-ray:
    • demonstrates chondrocalcinosis
    • useful in chronic gout to distinguish between osteoarthritis and rheumatoid arthritis changes
    • destructive changes may be an indication for urate lowering therapy


Management of Acute attack

Acute attack – prompt treatment works best

Suppress pain and reduce inflammation until acute flare has subsided.

NSAIDs see section 10.1 Drugs used in rheumatic diseases and gout

Are the drugs of choice in most patients with acute gout who do not have underlying health problems. Avoid NSAIDs in patients who have a history of peptic ulcer or GI bleeding, patients with renal insufficiency, patients with abnormal hepatic function, patients taking warfarin (selective COX-2 inhibitors can be used)

  • NSAIDs lasting 2 days after symptoms settle +/- PPI or

Colchicine see section 10.1 Drugs used in rheumatic diseases and gout

Although colchicine was once the treatment of choice for acute gout, it is now a second-line approach because of its narrow therapeutic window and risk of toxicity. It is contraindicated if GFR less than 30 and if there is active GI bleeding, main side effect (dose related) is diarrhoea


  • Prednisolone 20mg daily for 1 week then wean down over 2-3 weeks.

Follow up

Ask the patient to return for follow-up if there is no resolution of symptoms after 3-4 days and consider:

  • reviewing the diagnosis
  • checking compliance with medication
  • encouraging self-care strategies
  • increasing the dose of medication to maximum and adding paracetamol with or without codeine

If there is still no improvement in symptoms:

  • consider different medication or combining treatments; or
  • reconsider the diagnosis; or
  • seek specialist advice
  • Follow up the person 4-6 weeks after an acute attack of gout has resolved, and:
  • check the serum uric acid level
  • measure their blood pressure and take blood for:
    • fasting glucose, renal function, lipid profile
  • identify underlying conditions such as:
    • hypertension, diabetes, renal impairment
  • assess the person's overall cardiovascular risk
  • provide advice on risk factors such as:
    • obesity, diet, excessive alcohol consumption, exercise
  • consider prophylactic medication if a person is having two or more attacks of gout in a year
  • provide an advance prescription of effective treatment for future attacks of gout - immediate treatment of an acute attack is more effective that treatment started 24 hours later

Management of Recurrent attack

Lifestyle modifications (see patient information link below)

Reconsider precipitating drugs e.g. diuretics / aspirin / salicylates

Consider urate lowering treatment (e.g. allopurinol) if

  • 2 or more attacks per year
  • renal impairment (lowering urate is renoprotective)
  • urate stones
  • tophi
  • erosions on xray
  • need to continue diuretic therapy

Don't start urate lowering therapy until disease in remission

Give NSAIDs (+/- PPI) or colchicine (0.5mg per day) for a week before and the first 3-6 months of allopurinol to prevent a flare – a frequent cause of relapse is inadequate NSAID / colchicine protection


  • typical starting dose see section 10.1 Drugs used in rheumatic diseases and gout
  • reduce dose in renal impairment – 50mg - and slow cautious dose increases – (see BNF – see link below)
  • allopurinol hypersensitivity is rare but increased in renal impairment. Stop treatment if any rash develops and liaise with rheumatology

Explain this treatment is life long and may initially precipitate flares – continue the treatment

A recent BMJ article explains that allopurinol is often under-dosed and not given long term

Treat acute flares as above

Febuxostat (see section 10.1 Drugs used in rheumatic diseases and gout for cautions / contraindications)

If allopurinol intolerant or treatment not successful then consider febuxostat.

Please contact rheumatology with any clinical concerns

Follow up

If taking allopurinol, check the serum uric acid level and renal function every 3 months in the first year, then annually, and aim for a serum uric acid level below 300 micromol/L.

If taking febuxostat, use clinical judgement to decide if liver function tests need to be retested periodically.

If the person is still having frequent attacks of gout:

  • assess compliance with prophylactic medication or increase the dose if appropriate
  • review any trigger factors such as:
    • medication, trauma, diet, weight gain, excess alcohol consumption
  • provide a home supply of medication to use during an acute attack to minimize the impact on the person's functioning

Review cardiovascular risk factors and provide on-going lifestyle advice:

  • in a person with hypertension, stop diuretics during an acute attack and change to an alternative antihypertensive
  • in a person with heart failure, continue diuretics during an acute attack - if using a non-steroidal anti-inflammatory drug (NSAID) for pain relief, monitor renal function closely

Consider referral to secondary care, if the person is still having attacks despite all these measures.

Chapter 10.1 Drugs used in rheumatic diseases and gout.


Referral Criteria

Consider referral to secondary care, if the person is still having attacks despite the measures taken (see management).

Referral Instructions

Refer to Rheumatology

e-Referral Service

  • Specialty: Rheumatology
  • Clinic Type: Rheumatology
  • Service: DRSS-Western-Rheumatology-Devon CCG-15N

Referral Forms

Referral form

Supporting Information

Patient Information


Pathway Group

This guideline has been signed off on behalf of the Western Locality of NEW Devon CCG.

Publication date: July 2017


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