Acute Polyarthritis

Acute polyarthritis has a very wide differential diagnosis, presenting significant diagnostic difficulties. Where oligoarthritis (<5 joints affected) is the presenting feature, some of the causes of acute monoarthritis must be considered, the most important of which not to miss is septic arthritis (particularly that due to gonococcal infection which may affect several joints).¹ This article also considers conditions which may cause polyarthralgia that 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. The panoply of autoantibody tests available to aid diagnosis of rheumatological conditions can be misleading if not considered in the context of the clinical presentation.² They are best used to confirm a clinical suspicion, rather than as suggesters of a diagnosis. Conditions more normally 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 decide whether it is a chronic or one-off phenomenon. In some cases a definitive diagnosis may never be reached.³

See also Aching Joints, and Rheumatological History, Examination and Investigation.

• Demographic details such as age, sex, ethnic origin and occupation can give useful diagnostic clues.For example, Juvenile Chronic Arthritis is the commonest arthritis in children.⁴
• Family history may be present in cases of RA, seronegative arthropathies and osteoarthritis.
• Pain is not often discriminatory in diagnostic terms. Speed of onset may help - gout tends to come on abruptly whereas rheumatoid arthritis (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, sarcoidosis, SLE, Lyme disease or endocarditis.
• Pattern of joint involvement is very useful in suggesting a diagnosis. For example, osteoarthritis of the hand affects the DIP and PIP joints but spares the 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 osteoarthritis. 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, 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 can cause a lupus like syndrome and there have been reports of polyarthralgia associated with omeprazole.⁵
• Systemic symptoms should also be sought e.g. fever and weight loss.⁶
• Are there any symptoms of abdominal or respiratory disease?

• Check temperature.
• Nail changes e.g. pitting may suggest psoriatic arthropathy.
• Look at eyes for signs of inflammation.
• Check major lymph nodes for evidence of lymphadenopathy.
• Check skin for rashes and evidence of vasculitis.⁷ 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 rheumatic fever.
• 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 and tenderness and synovial thickening. Are there 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 but may give some indication as to the degree of damage. Also examine the structures around the joint and determine if the symptoms are intra- or peri-articular.

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

• Viral infections - Parvovirus B19, Enteroviruses, Adenoviruses, EBV, Coxsackie, CMV, Hepatitis viruses especially B, Mumps, rubella, HIV
• Direct bacterial infections - Gonococcal infection, S. Aureus, Streptococci, Gram-negative organisms, Bacterial endocarditis
• Reactive to bacterial infection - Gonococcal infection, Campylobacter, Chlamydia, Salmonella, Shigella, Yersinia, Rheumatic fever (Group A streptococci), Reiter's syndrome
• Other infections - Lyme disease (Borrelia burgdorferi), Tuberculosis (Mycobacterial), Fungal infection, Weil's disease (leptospirosis), Whipple's disease (Tropheryma whippelii)
• Crystal arthropathy/metabolic disease - Gout (urate), Pseudogout (calcium pyrophosphate), Hydroxyapatite, Wilson's disease, Haemochromatosis, Amyloidosis, Hyperlipidaemia, Multicentric reticulohistiocytosis, Alkaptonuria
• Systemic rheumatological disease - RA, SLE, Polymyositis/dermatomyositis, Juvenile chronic arthritis, Scleroderma, Sjögren's syndrome, Behçet's syndrome, Familial mediterranean fever, fibromyalgia
• Systemic vasculitic disease - see vasculitis, e.g. Henoch-Schonlein purpura, Polyarteritis nodosa, Wegener's granulomatosis, Giant cell arteritis, Hypersensitivity vasculitis
• Spondyloarthropathies - Ankylosing spondylitis, Psoriatic arthritis, Enteropathic arthropathy (Inflammatory bowel disease-associated)
• Endocrine disease - Hyperparathyroidism, Hyperthyroidism, Hypothyroidism, Acromegaly
• Malignancy - Metastatic cancer, Multiple myeloma
• Degenerative/structural - Primary generalised (erosive) osteoarthritis, Secondary osteoarthritis, Neuropathic joints
• Miscellaneous - Sarcoidosis, Fibromyalgia, Hypertrophic Pulmonary Osteoarthropathy, Hypermobility syndromes, (e.g. Ehlers-Danlos or Marfan's), Osteomalacia, Drug/serum reactions, Polymyalgia rheumatica, Sweet's syndrome, Palindromic rheumatism,

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. See acute monoarthritis for a table of synovial fluid findings in the commoner causes of joint inflammation.

• Urinalysis - indicates any renal involvement.
• Bloods - 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 non-specific or insensitive.³ They should be interpreted in the context of the clinical presentation, preferably with specialist rheumatological input for the less common markers.
• Radiology - X-rays play a variable role in their contribution to diagnosis but are a useful first line investigation. Other imaging modalities may need to be conducted with rheumatological/radiological advice.

Directed at the underlying diagnosis. See the links to the individual diagnoses for detail. Symptomatic treatment of inflammatory conditions with NSAIDs should be considered whilst awaiting the evolution of an arthritis, where there are no contraindications 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.