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This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Arthritis article more useful, or one of our other health articles.

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Acute polyarthritis has a very wide differential diagnosis, presenting significant diagnostic difficulties. Where oligoarthritis (fewer than five joints affected) is the presenting feature, some of the causes of acute monoarthritis must be considered, of which the most important not to miss is septic arthritis (particularly that due to gonococcal infection which may affect several joints).

This article also considers conditions which may cause polyarthralgia which can present in a similar fashion to the inflammatory diseases.

Careful clinical assessment should give a reasonable differential diagnosis which can be further narrowed down by appropriate investigations. Autoantibody tests used to aid diagnosis of rheumatological conditions can be misleading if not considered in the context of the clinical presentation. They are best used to confirm a clinical suspicion, rather than as suggesters of a diagnosis.

Conditions more commonly considered to be chronic and indolent can present floridly in the acute phase. It can take time for a disease to evolve into its classical pattern and for the decision to be reached as to whether it is a chronic condition or a one-off phenomenon. In some cases a definitive diagnosis may never be reached[1].

See also the separate Aching Joints - Assessment, Investigations and Management in Primary Care and Rheumatological History, Examination and Investigations articles.

  • Details such as age, sex, ethnic origin and occupation can give useful diagnostic clues. For example, juvenile idiopathic arthritis is the most common arthritis in children.
  • Family history may be present in cases of rheumatoid arthritis (RA), seronegative arthropathies and osteoarthritis (OA).
  • Pain is not often discriminatory in diagnostic terms. Speed of onset may help - gout tends to come on abruptly, whereas RA is usually more gradual. Similarly, gout tends to cause very severe, excruciating pain.
  • Diurnal variation of symptoms may give useful clues. An inflammatory arthritis tends to be worse on waking and eases as the day goes on. Mechanical pain tends to have the opposite effect.
  • Ask about morning stiffness and joint swelling.
  • Migratory arthritis (flitting from joint to joint over a period of days) might suggest gonococcal infection, rheumatic fever (RF), sarcoidosis, systemic lupus erythematosus (SLE), Lyme disease or bacterial endocarditis.
  • Pattern of joint involvement is very useful in suggesting a diagnosis. For example:
    • OA of the hand affects the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints but spares the metacarpophalangeal (MCP) joints.
    • RA affects the MCP and PIP joints but spares the DIP joints.
    • Psoriatic arthritis, crystal arthropathies and sarcoidosis can affect all these joints.
    • Large weight-bearing joints and facet joints of the spine are often affected by OA.
    • Axial involvement in younger patients suggests a seronegative arthropathy such as ankylosing spondylitis or inflammatory bowel disease-associated arthropathy.
  • Symmetrical joint involvement tends to occur in systemic syndromes such as RA, SLE, viral arthritis and drug/serum sickness reactions.
  • In asymmetrical joint involvement consider gout, psoriatic arthritis and reactive arthritis.
  • Extra-articular symptoms should be asked about and can aid diagnosis. The eyes, parotid glands, skin, mouth, genitals and muscles can all be affected by rheumatological diagnoses.
  • Take a full drug history - some drugs (eg, hydralazine, procainamide, quinidine and minocycline) can cause a lupus-like syndrome[2]and there have been reports of a variety of drugs associated with polyarthralgia (eg, moxifloxacin)[3].
  • Systemic symptoms should also be sought - eg, fever and weight loss.
  • Note whether there any other associated presenting symptoms - eg, abdominal or respiratory disease.
  • Check temperature.
  • Nail changes (eg, pitting) may suggest psoriatic arthropathy.
  • Look at the eyes for signs of inflammation.
  • Check major lymph nodes for evidence of lymphadenopathy.
  • Check the skin for rashes (eg, psoriasis, SLE) and evidence of vasculitis. Feel extensor aspects of forearms for nodules. Check shins for evidence of erythema nodosum.
  • Cardiac examination - listen for murmurs if there is reason to suspect RF.
  • Abdominal examination - may reveal evidence of hepatomegaly and/or splenomegaly.
  • Examine other systems as indicated by the history and clinical hypotheses.
  • Joint examination:
    • Look for signs of inflammation in the joint, such as heat, tenderness and synovial thickening.
    • Establish whether there are symmetrical or asymmetrical joints involved.
    • Active and passive movements of affected joints and the degree of pain and/or crepitus may also be helpful. However, crepitus and pain will not differentiate between inflammatory and non-inflammatory causes of joint pain. They may, however, give some indication as to the degree of damage.
    • Also examine the structures around the joint and determine if the symptoms are intra-articular or periarticular.
Discriminating features of common causes of polyarthritis[1]
Development over time
Pattern joint involvement
Axial involvement
Extra-articular manifestations/other features
Rheumatoid arthritis (RA)
ChronicYesSmall and large jointsYesNeckNodules
Osteoarthritis (OA)
ChronicNoWeight-bearing joints, proximal interphalangeal (PIP) joint, distal interphalangeal (DIP) joint, first carpometacarpal (CMC) jointVariableNeck and lower backNone, Heberden's nodes (distal) and Bouchard's nodes (proximal)
Systemic lupus erythematosus (SLE)
ChronicYesSmall jointsYesNoMalar rash, mouth ulcers, pleuritis, pericarditis
Psoriatic arthritis
ChronicYesLarge and small jointsVariableVariablePsoriatic rash, dactylitis, nail changes, tendonopathy
Human parvovirus B19 infection
Acute and remittingYesSmall jointsYesNoLacy rash, malar rash
Ankylosing spondylitis
ChronicYesLarge jointsYesYesIritis, aortic regurgitation, tendonopathy

The diagnoses below are not exhaustive but cover the vast majority of causes of polyarthritis.

Differential diagnosis
Viral infections[4]
Direct bacterial infections
Other infections
Reactive to bacterial infection
Crystal arthropathy/metabolic disease
Systemic rheumatological disease
Systemic vasculitic disease
Endocrine disease

Where there is any suspicion of septic arthritis, immediate aspiration of synovial fluid should be carried out. Synovial fluid analysis may play a role in diagnosis of crystal arthropathies and inflammatory conditions but results need to be carefully interpreted in context. The table below shows the findings in the more common causes of arthritis:

Synovial fluid changes in common causes of monoarthritis 
  • Appearance: clear, viscous fluid
  • WBC count (cells per 10-6/L): 0-200
  • Crystals: nil
  • Culture: sterile
Septic arthritis
  • Appearance: turbid, low viscosity
  • WBC count (cells per 10-6/L): 50,000-200,000 neutrophils
  • Crystals: nil
  • Culture: positive (in some cases)
Gout (uric acid)
  • Appearance: clear, low viscosity
  • WBC count (cells per 10-6/L): 500-200,000 neutrophils
  • Crystals: needle-shaped and negatively birefringent
  • Culture: sterile
Pseudogout (pyrophosphate)
  • Appearance: clear, low viscosity
  • WBC count (cells per 10-6/L): 500-10,000 neutrophils
  • Crystals: block-shaped and positively birefringent
  • Culture: sterile
Inflammatory - eg, rheumatoid arthritis
  • Appearance: turbid, yellowish-green (chicken soup), low viscosity
  • WBC count (cells per 10-6/L): 2,000-100,000 neutrophils
  • Crystals: nil
  • Culture: sterile
  • Appearance: large volume, normal viscosity, may be blood-stained if trauma/haemarthrosis
  • WBC count (cells per 10-6/L): 0-2,000 mononuclear
  • Crystals: usually none (5% have pyrophosphate crystals)
  • Culture: sterile
  • Blood tests - FBC, ESR, CRP and U&E are useful screening investigations which give diagnostic clues.
  • Autoantibodies - can help to confirm a diagnosis but are often relatively nonspecific or insensitive[6]. They should be interpreted in the context of the clinical presentation, preferably with specialised rheumatological input for the less common markers.
  • Rheumatoid factor - if synovitis on clinical examination. Consider measuring anti-cyclic citrullinated peptide (anti-CCP ) antibodies in adults with suspected RA if they are negative for rheumatoid factor[7].
  • Radiology - X-rays play a variable role in their contribution to diagnosis but are a useful first-line investigation. X-ray the hands and feet in adults with suspected RA and persistent synovitis[7]. Other imaging modalities may need to be conducted with rheumatological/radiological advice.
  • Urinalysis - indicates any renal involvement.
  • Joint aspiration may be helpful in establishing the diagnosis in secondary care.

Directed at the underlying diagnosis. See the links to the individual diagnoses for detail.

Symptomatic treatment of inflammatory conditions with non-steroidal anti-inflammatory drugs should be considered whilst awaiting the evolution of an arthritis, where there are no contra-indications or significant drug interactions.

Where there is a significant inflammatory illness as revealed by clinical severity and CRP/ESR, etc, early advice for disease-modifying interventions can significantly reduce joint pathology in some conditions.

If in doubt, seek advice on the appropriate course.

For patient with possible RA, the National Institute for Health and Care Excellence (NICE) recommends[7]:

  • Refer for specialist opinion any adult with suspected persistent synovitis of undetermined cause.
  • Refer urgently (even with a normal acute-phase response, negative anti-CCP antibodies or rheumatoid factor) if any of the following apply:
    • The small joints of the hands or feet are affected.
    • More than one joint is affected.
    • There has been a delay of three months or longer between onset of symptoms and seeking medical advice.

Further reading and references

  1. Mies Richie A, Francis ML; Diagnostic approach to polyarticular joint pain. Am Fam Physician. 2003 Sep 1568(6):1151-60.

  2. Dalle Vedove C, Simon JC, Girolomoni G; Drug-induced lupus erythematosus with emphasis on skin manifestations and the role of anti-TNFalpha agents. J Dtsch Dermatol Ges. 2012 Dec10(12):889-97. doi: 10.1111/j.1610-0387.2012.08000.x. Epub 2012 Sep 3.

  3. Torres JR, Bajares A; Severe acute polyarthritis in a child after high doses of moxifloxacin. Scand J Infect Dis. 200840(6-7):582-4.

  4. Holland R, Barnsley L, Barnsley L; Viral arthritis. Aust Fam Physician. 2013 Nov42(11):770-3.

  5. Serratrice J, Disdier P, Colson P, et al; Acute polyarthritis revealing hepatitis E. Clin Rheumatol. 2007 Nov26(11):1973-5. Epub 2007 Mar 6.

  6. Pujalte GG, Albano-Aluquin SA; Differential Diagnosis of Polyarticular Arthritis. Am Fam Physician. 2015 Jul 192(1):35-41.

  7. Rheumatoid arthritis in adults: management; NICE Guideline (July 2018 - last updated October 2020)

  8. Siva C, Velazquez C, Mody A, et al; Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Am Fam Physician. 2003 Jul 168(1):83