Indian J Pediatr (2010) 77:1005–1010
DOI 10.1007/s12098-010-0163-5
SYMPOSIUM ON PEDIATRIC RHEUMATOLOGY-I
Approach to Polyarthritis
Surjit Singh & Sonia Mehra
Received: 13 July 2010 / Accepted: 14 July 2010 / Published online: 24 August 2010
# Dr. K C Chaudhuri Foundation 2010
Abstract A child with polyarthritis is always a diagnostic
challenge for the treating physician. By definition, polyarthritis,
taken in context as a subgroup of juvenile idiopathic arthritis, is
defined as inflammation of more than 4 joints on physical
examination. Though the exact incidence and prevalence of
polyarthritis in childhood is not known, it is not uncommon in
pediatric practice. Polyarthritis can be a clinical manifestation
of diverse disease processes and the differential diagnosis is
understandably very broad. It can be caused directly by an
infectious agent or indirectly by immune mechanisms, may be
a component of a systemic disease process or may be
idiopathic. The presentation can be acute or chronic. It can
represent a benign self limiting illness requiring no specific
treatment or may be a severely disabling condition with
significant morbidity and, in some cases, even mortality. While
in some situations it may be possible to arrive at a provisional
clinical diagnosis right at the outset, in others the diagnosis
gradually evolves over a period of time. As in most other
arthritides, the most important aspects of the diagnosis are a
thorough history and a detailed clinical examination. Relevant
laboratory investigations can help in facilitating the diagnosis
but can often also mislead the treating physician. Hereby we
present a clinical approach to a child with polyarthritis.
Keywords Polyarthritis . Children . Clinical approach
“When an arthritis patient walked in the front door I
wanted to walk out the back one”—Sir William Osler
(1849–1919)
Principles and Practice of Medicine, 1892
S. Singh (*) : S. Mehra
Pediatric Allergy Immunology Unit, Advanced Pediatrics Centre,
Postgraduate Institute of Medical Education and Research,
Chandigarh 160012, India
e-mail: surjitsinghpgi@rediffmail.com
Introduction
Although acute monoarthritis (as for instance septic
arthritis) is usually considered to be a medical emergency
[1], it is not often realized that patients with polyarthritis
also need to be evaluated promptly to ensure timely
management [2]. Delays in diagnosis and/or treatment
may result in significant morbidity, as for example in
rheumatic fever and Kawasaki disease [3]. It cannot be
overemphasized enough that the most important clues to
underlying aetiology in a patient with polyarticular disease
are found not in the investigations but in the clinical history
and physical examination. Some investigations (e.g. radio-
graphs of joints) are commonly done but may have little or no
role in the initial assessment of the patient [2, 4].
Polyarticular joint disease has multi-factorial etiology.
It may present acutely as in self limiting viral illnesses or
it can be the beginning of a chronic sinister disease. The
underlying etiological process can be infectious or post-
infectious, a rheumatological disease or a manifestation of
systemic disease. The disease may evolve over days or
sometimes weeks, thereby making the diagnosis difficult
at the time of presentation [4–11] (Table 1). Viral
infections (for e.g. Parvovirus B19) are often associated
with a self-limiting symmetrical arthritis of small joints.
Septic polyarthritis caused by direct invasion of the joint by
microbes can occur in disseminated staphylococcal and
streptococcal infections, gram negative sepsis or bacterial
endocarditis. Reactive arthritis, a sterile arthritis mediated by
immune mechanisms, is usually seen after genitourinary
(Chlamydia) or gastrointestinal (salmonella, shigella, yersinia
or campylobacter) infections. It is said that arthritis persisting
for more than 6 weeks usually rules out an infective pathology
[9, 10]. Polyarticular juvenile idiopathic arthritis (JIA),
polyarthritis associated with systemic lupus erythematosus
(SLE) and psoriatic arthritis usually present insidiously and
1006
Table 1 Differential diagnosis
of polyarthritis Etiology
Viral
Bacterial
Other infections
Parainfectious
(reactive)
Rheumatalogical
Systemic vasculitides
Spondyloarthropathies
Miscellaneous
should be considered in the differential diagnosis of such a
patient.
History
Identifying the cause of polyarthritis may initially look
difficult to the uninitiated. However, clinical clues in
patient demographics, disease chronology, inflammatory
nature, progression, distribution of joint involvement and
extra-articular manifestations help narrow the diagnostic
possibilities [2].
Age At the onset of the disease may give clues to the
diagnosis. Polyarticular JIA (rheumatoid factor negative),
Kawasaki disease and Henoch Schonlein purpura (HSP)
usually present in early childhood. In mid-childhood, juvenile
psoriatic arthritis, Juvenile Dermatomyositis (JDMS) and
Polyarteritis Nodosa (PAN) have their peak frequencies.
Juvenile ankylosing spondylitis (JAS) and SLE typically
present in late childhood or early adolescence. Rheumatoid
factor positive polyarticular JIA, mimicking the clinical
profile of adult RA, usually presents only after the age of
10 years. Disorders like gout and crystal deposition disease are
extremely uncommon in children [11–13].
Sex While many rheumatological disorders (e.g. SLE,
polyarticular JIA) have a predilection for girls, there are
others (e.g. vasculitides like KD and PAN; spondyloarthro-
pathies like inflammatory bowel disease and JAS) which
are more common in boys [14, 15].
Onset of Disease and Duration While some arthritides may
have an acute onset (e.g. septic arthritis and arthritis
associated with KD/HSP) others may have a subacute or
chronic insidious course as typically seen in polyaticular
Indian J Pediatr (2010) 77:1005–1010
Causative agent
Parvovirus B19, Enteroviruses, Adenoviruses, Mumps, Rubella, Varicella zoster
virus, Hepatitis B, Coxsackie virus, Cytomegalovirus, EBV, HIV.
Staphylococcal and streptococcal infections, Neisseria gonorrhae, Hemophilus
influenzae; Bacterial endocarditis.
Tuberculosis, Leptospirosis, Fungal infections, Brucellosis
HIV, Group A streptococcal infections, Salmonella, Shigella, Yersinia,
Campylobacter, Mycoplasma, Chlamydia.
Juvenile idiopathic arthritis (JIA), Systemic lupus erythematosus (SLE),
Juvenile dermatomyositis (JDMS), Behcet syndrome.
Henoch-Schonlein purpura (HSP), Kawasaki disease (KD), Polyarteritis
nodosa (PAN), Wegener’s granulomatosis
Juvenile ankylosing spondylitis (JAS), Psoriatic arthritis
Enteropathic arthritis.
Sarcoidosis, Drug/serum sickness reactions
JIA or sarcoidosis. Polyarthritis of less than 6 weeks
duration is seen in self limiting viral arthritides, rheumatic
fever or reactive arthritis [12, 13]. It may sometimes be
prudent not to give a label in the first few weeks of the
illness when the disease process is still evolving.
Past History A transient episode of heel or back pain
(indicating enthesitis) or an episode of painful red eye with
visual loss (indicating acute uveitis) may unmask the
inflammatory back pain in JAS [13, 15]. History of recent
diarrhea, acute conjunctivitis, urethritis, and fever with or
without rash may give a clue to reactive arthritis [10, 16].
Patients with systemic onset JIA may present with pyrexia
of unknown origin and give history of having received
multiple courses of antimicrobials. In our experience this is
not an uncommon occurrence.
Family History Although Mendelian inheritance is not
usually seen in inflammatory polyarthritis, familial cluster-
ing of cases can be seen in ankylosing spondylitis,
inflammatory bowel disease and psoriatic arthritis. The
latter condition is especially intriguing because clinical
manifestations of psoriasis can be subtle and very variable
amongst the family members [15].
Physical Examination
Articular Involvement
Examination involves determining not only which joints are
involved at any one time, but determining over time if
possible, the evolution of joint involvement.
Clinical approach to a child with polyarthritis essentially
revolves around recognition of the pattern of joint involve-
ment. It may not always be possible to give a specific diagnostic
Indian J Pediatr (2010) 77:1005–1010 1007

Table 2 Common patterns of involvement in children

Disease Clinical presentation Pattern Symmetry Axial involvement

Viral arthritis Acute Small Joints Symmetrical No

Polyarticular JIA Chronic Small and large Symmetrical or asymmetrical No
JAS Chronic Large Asymmetrical Yes
Psoriatic arthritis Chronic Small and large Usually asymmetrical Yes / No
SLE Chronic Small Symmetrical No
Reactive arthritis Acute Large Asymmetrical Yes / No

label at the first instance. The treating clinician has to identify
the following components in evolution of the disease:
1. Evolution of the joint involvement
Progression of joint involvement can follow one of
the following patterns [11, 17]:
Migratory—symptoms are present in one joint for
a few days and then remit, only to reappear in
some other joint as classically seen in rheumatic
fever and gonococcal arthritis. Joint involvement
can occur over hours in rheumatic fever or over
days in gonococcal arthritis.
Additive—New joints are progressively involved
while initial joints are still symptomatic with many
joints being affected at the same time as seen in
SLE, JIA and psoriatic arthritis.

Table 3 Physical signs to be looked for in a child with polyarthritis [5, 11, 13, 23]

System involved Physical findings Systemic disease

Eye Anterior or posterior uveitis, non exudative conjunctivitis, JIA, JAS, KD, Sarcoidosis, Reactive
Keratoconjuctivitis arthritis Sjogrens syndrome
Skin/Mucosa
Oral cavity Oral ulcers, straw berry tongue SLE, KD, Bechet syndrome
Skin Malar rash, discoid rash, macular rash, heliotrope rash, Gottorn’s SLE, Rheumatic fever JIA, JDMS,
papules, palpable purpura, petechaie, Erythema nodosum, Systemic vasculitides, Sarcoidosis,
Erythema marginatum, leg ulcers, Raynaud phenomenon, edema HSP, Parvovirus infection,
of hands and feet, perianal desquamation, slapped cheek Reactive arthritis
appearance, genital ulcers
Nails and hair Alopecia, nail pitting, onycholysis, clubbing SLE, Psoriasis, IBD
Musculoskeletal System
Muscles and joints Proximal muscle weakness, muscle tenderness, muscle JDMS, JAS, JIA, Psoriatic arthritis
contractures, enthesitis, bursitis, dactylitis ankylosis
Hematological System
CBC Leucocytosis, thrombocytosis, thrombocytopenia, eosinophilia JIA, SLE, Sarcoidosis
Vascular system Gangrene, stroke SLE, APLA Syndrome
Lymphatic system Lymphadenopathy SLE, KD
Renal System
Kidneys Nephritis, nephrotic syndrome, hypertension, urinary JIA, KD, SLE, PAN, HSP
sediment, sterile pyuria, amyloidosis, RPGN and ESRD
Nervous system
Central nervous system Stroke, seizures, focal deficits, psychosis, chorea, RF, SLE, PAN, Bechet syndrome
blindness, aseptic meningitis, pseudotumor cerebri
Peripheral nervous system Mononeuritis complex, polyneuropathy PAN, SLE Chrugg strauss syndrome
Respiratory System
Paranasal sinuses Acute or chronic sinusitis Wegener’s granulomatosis
Lungs Hilar adenopathy, pulmonary infiltrates, Pulmonary Sarcoidosis, PAN
haemorrhage and pulmonary hypertension
Cardiovascular System
Heart Myocardial dysfunction, endocarditis, pericardial effusion, Mitral RF, JAS, SLE, PAN, Bacterial
regurgitation and stenosis, Aortic regurgitation, new murmurs endocarditis

RF rheumatic fever, JIA juvenile idiopathic arthritis, JAS juvenile ankyolising spondyolitis, HSP henoch schonlein purpura, KD Kawasaki disease,
JDMS juvenile dermatomyositis, SLE systemic lupus erythematosus, PAN polyarteritis nodosa, APLA antiphospholipid antibodies
1008 Indian J Pediatr (2010) 77:1005–1010

Table 4 Laboratory investigations in a child with polyarthritis

Investigation Abnormality detected Comments

Markers of inflammation ↑ ESR, ↑ CRP, ↑ Globulins, thrombocytosis ESR and CRP elevation usually indicate activity but ESR may not
always be elevated in rheumatic diseases
Hemogram Normocytic normochromic anemia, SLE may have leucopenia and thrombocytopenia at presentation
leucocytosis, thrombocytosis, Eosinophilia,
haemolytic anemia (DCT+)
Urine routine Urinary sediment, sterile pyuria, hematuria Sterile pyuria commonly seen in JIA and KD;
and proteinuria should not be mistaken for UTI
Radiology of the joint X-rays, CT scans or MRI Not usually required in acutely painful joint; may
not be informative in acute stage.
Synovial fluid Synovial fluid in JIA can also have a Indicated only if there is a diagnostic problem; in addition to Gram
analysis/Biopsy markedly polymorphonuclear response; stain, pyogenic and mycobacterial cultures are sent. Biopsy can
should not be mistaken for septic arthritis be aided by direct vision under arthroscopy
Specific investigations RF, anti CCP antibodies, HLA B27, Polyarticular disease can be RF +/−, ANA is usually positive
ANA and ANCA in SLE, HLA B27 for Juvenile spondyloarthropathies and
reactive arthritis, ANCA for systemic vasculitides
Other investigations RFT, LFT, X-ray, ASO titres, Throat swab, Baseline metabolic profile should be done in all
HIV, Viral serologies, ECHO patients and other investigations are disease specific

Intermittent—Joint involvement appears and dis-
appears with completely asymptomatic periods in
between, as seen in reactive arthritis.
2. Topography and distribution
Typically joint involvement can be axial (spine,
centrally located joints as sacroiliac joint, sternoclavicular
or manubriosternal joint), peripheral joints (in the
extremities) or root joints (overlap between axial and
peripheral joints e.g. shoulder and hip joint).
While involvement of the axial skeleton is typical of
the spondyloarthropathies, it is extremely uncommon in
disorders like SLE and systemic vasculitides. Combined
patterns of involvement can be seen in polyarticular or
systemic JIA. A young adult who has chronic low back
pain and peripheral asymmetric arthritis probably has
one of the spondyloarthropathies like JAS, psoriatic
arthritis, enteropathic associated arthritis or reactive
arthritis [18].
3. Distribution
Is the joint involvement symmetric or asymmetric?
Symmetric—Inflammatory synovitis of small as
well as large joints of extremities in symmetrical
distribution in both upper and lower limbs is
typical of JIA and SLE.
Asymmetric—Asymmetrical involvement of large
joints of lower extremities (for e.g. ankle / knee) is
typical of reactive arthritis.
4. Is any particular joint involved?
The physician should assess if the joint involvement
is characteristic of a particular disorder. This assess-
ment should begin as soon as the child walks into the
clinic. For example acute dactylitis or distal interpha-

Table 5 Treatment of commonly encountered polyarthritis in children

Common causes of polyarthritis Specific therapy Comments

Infectious/ Parainfectious Viral infections are often self limiting; specific Patients with Rheumatic fever require long term penicillin
a) Viral antimicrobials for bacterial infections; NSAIDs prophylaxis reactive arthritis commonly seen in older
b) Bacterial for a few weeks in reactive arthritis children and adolescents
c) Reactive
Rheumatological disorders NSAIDs and/or steroids and immunosuppressive Physiotherapy and occupational therapy as important as
therapy depending on the specific disorder drug therapy
Systemic Vasculitides Immunoglobulin in KD, NSAIDs/steroids in HSP Immunoglobulin therapy in KD can prevent long term
and other vasculitides morbidity; prompt administration of steroids in lupus
can be life saving
Miscellaneous Supportive and definitive treatment depending Disease may evolve in time in any category and patients
on aetiology need follow up
Indian J Pediatr (2010) 77:1005–1010
langeal involvement raises the strong suspicion of
psoriatic arthritis [15]. Family history of a near relation
having psoriasis further corroborates the diagnosis.
Enthesitis (i.e. Inflammation at the site of attachment
of ligaments, tendons and fascia to the bone) is typical
of the juvenile spondyloarthropathies [18]. It must,
however, be noted that there can be considerable
overlaps in the patterns of joint involvement and the
overall clinical picture must not be ignored.
5. Is there a joint deformity?
Arthritis can be deforming or non-deforming. Joint
deformities usually indicate a long standing or aggres-
sive disease. Deforming arthritis is typically seen in
polyarticular JIA. Early initiation of anti-inflammatory
therapy can help prevent some of these deformities.
The arthritis associated with SLE and inflammatory
bowel disease is usually non-deforming [19] (Table 2).
Extra-articular Involvement
Inflammatory arthritis may be associated with systemic
features and many systemic diseases have musculoskeletal
presentations. These extraarticular manifestations may
provide many valuable clues to the underlying etiology
(Table 3) [20, 21].
Laboratory Investigations
It is said that 80% of the rheumatological diagnosis comes
from clinical history, 15% from examination and only 5%
from investigation. This aphorism is applicable to the clinical
approach to polyarthritis as well. Laboratory investigations, by
themselves, have very little role in arriving at a diagnosis and
one should never fall in the trap of treating the investigation
rather than the patient. As most of the rheumatological tests
lack the desired specificity, results should always be inter-
preted in the context of a given patient [22] (Table 4). Further,
the tendency to send for ‘routine’ panels of tests (e.g.
“arthritis” panel, “lupus” panel) without keeping the patient’s
clinical picture in perspective can never be justified.
Management
Management necessarily has to be multidisciplinary with
involvement of the physiotherapist and the occupational
therapist (Table 5). One has to address parental concerns for
the disease and the issues regarding its prognosis, medica-
tions, and school absenteeism [23]. Symptomatic relief
should be provided while the child is being evaluated.
Specific therapy, however, depends on the underlying
etiology of the arthritis.
1009
Conclusion
Polyarthritis could be a benign self-limiting illness, the
beginning of a serious chronic illness resulting in significant
morbidity or a rheumatological emergency requiring urgent
intervention. While the differential diagnosis can be very
broad, a presumptive diagnosis with regard to the underlying
etiology can often be made by careful attention to the clinical
history and physical examination. Laboratory investigations
must always be directed by the clinical presentation. Manage-
ment is tailored to the requirements of a given patient.
Conflict of interest None
References
1. Baker DG, Schumacher HR. Acute monoarthritis. N Engl J Med.
1993;329:1013–20.
2. Mies Richie A, Francis ML. Diagnostic approach to polyarticular
pain. Am Fam Physician. 2003;68:1151–60.
3. Special Writing Group of the Committee on Rheumatic Fever,
Endocarditis, and Kawasaki Disease of the Council on Cardio-
vascular Disease in the Young of the American Heart Association.
Guidelines for the diagnosis of rheumatic fever. JonesCriteria,
1992 update [published correction appears in JAMA.1993; 269(4):
476]. JAMA 1992;268(15):2069–73.
4. Allen R. Differential diagnosis of arthritis in childhood. Baillieres
Clin Pediatr. 1993;1:665–94.
5. Khubchandani RP, D’Souza S. Initial evaluation of a child with
arthritis—an alogrithmic approach. Indian J Pediatr. 2002;69
(10):875–80.
6. Klinkhoff A. Rheumatology: 5. Diagnosis and management of
inflammatory polyarthritis. CMAJ 2000;162:1833–8.
7. Meador R, Schmacher HR. Evaluating and treating patients with
polyarthritis of recent onset. Hosp Physician. 2003;39:37–45.
8. Pinals RS. Polyartrits and fever. New Engl J Med. 1994;330:769–74.
9. Rose CD, Eppes SC. Infection related arthritis. Rheum Dis Clin
North Am. 1997;23:677–95.
10. Leirisalo-Repo M. Early infection and arthritis. Curr Opin
Rheumatol. 2005;17(4):433–9.
11. Malaviya A. Approach to the patient with polyarthritis. In: Rao
URK, eds. Manual of rheumatology. 3rd ed. Indian Rheumatology
Association; 2009. 11–20.
12. Miller ML. Evaluation of a suspected rheumatic disease. In:
Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson
textbook of pediatrics. 18th ed. Philadelphia: Elsevier Saunders;
2007. 995–7.
13. Cassidy JT, Petty RE. Polyarthritis. In: Cassidy JT, Petty RE,
Laxer RM, Lindsley CB, editors. Textbook of pediatric rheuma-
tology. 5th ed. Philadelphia: Elsevier Saunders; 2005. p. 261–73.
14. Sathanathan R, David J. The adolescent with rheumatic disease.
Arch Dis Child. 1997;77:355–8.
15. Burgos-Vargas R. Spondyloarthropathies and psoriatic arthritis in
children. Curr Opin Rheumatol. 1993;5:634–43.
16. Townes JM. Reactive arthritis after enteric infection in the United
States: the problem of definition. Clin Infect Dis. 2010;50(2):247–54.
17. Hubscher O. Pattern recognition in arthritis In: Kippel JH, Dieppe
PA, editors. Rheumatology. 2nd ed. Mosby International; 1998; 2:
p. 3.1–3.6.
18. McGonagle D, Gibbon W, Emery P. Classification of inflamma-
tory arthritis by enthesitis. Lancet 1998;352:1137–40.
1010
19. Martel W, Holt JF, Cassidy JT. Roentgenologic manifestations of
juvenile rheumatoid arthritis. Am J Roentgenol Radium Ther Nucl
Med. 1962;88:400–42.
20. Baldassano VF. Ocular manifestations of rheumatic diseases. Curr
Opin Ophthalmol. 1998;9:85–8.
21. Griffiths ID. Extra- articular features of rheumatic diseases. In:
Maddison PJ, Isenberg DA, Woo P, Glass DN, eds. Oxford
Indian J Pediatr (2010) 77:1005–1010
textbook of rheumatology. 2nd ed. London: Oxford University
Press; 1998. 169–79.
22. Kunnamo I, Kallio P, Pelkonen P, Hovi T. Clinical signs and
laboratory tests in the differential diagnosis of arthritis in children.
Am J Dis Child. 1987;141:34–40.
23. Singh S. Chronic arthritis: current perspectives [editorial]. Indian
Pediatr. 2003;40:393–7.