Viral Arthritis

Viral arthritis refers to joint inflammation occurring as a direct or immune-mediated consequence of viral infection, generally self-limiting and distinct from bacterial septic arthritis in both course and management.

Common causative viruses include parvovirus B19 (particularly in adult women, often coinciding with or shortly after the classic "slapped cheek" rash in children but frequently presenting with arthralgia alone in adults, without a preceding rash), rubella (both wild-type infection and, historically, live attenuated vaccine), hepatitis B and C (often accompanying an immune complex mediated prodromal phase, alongside urticaria), chikungunya (notable for often severe, debilitating, and sometimes persistent polyarthralgia that can last months to years), and, less commonly, mumps, HIV seroconversion, and alphaviruses more broadly (Ross River virus, Sindbis virus in endemic regions).

Typically a symmetric, small joint polyarthralgia or polyarthritis (hands, wrists, knees, ankles) developing acutely, often alongside or shortly after a viral prodrome (fever, malaise, rash, lymphadenopathy).

Unlike septic arthritis, joints are generally not markedly hot, and systemic toxicity is usually mild to moderate rather than severe.

Parvovirus B19 arthropathy in adults can mimic early rheumatoid arthritis clinically (symmetric small joint involvement, morning stiffness) but typically resolves within weeks, though a subset of patients have more prolonged symptoms.

Chikungunya arthralgia is often disproportionately severe relative to objective joint swelling, and can become chronic in a meaningful minority.

Primarily clinical, guided by the accompanying features and epidemiological context (recent viral illness, rash, relevant travel history, or exposure).

Specific serology (parvovirus B19 IgM, hepatitis B/C serology, chikungunya IgM/PCR depending on timing) confirms the likely causative virus where relevant to management or where the presentation is atypical.

Joint aspiration is reserved for cases where septic arthritis cannot be confidently excluded (monoarticular, markedly hot joint, or significant systemic toxicity), given the very different management urgency, following the principles in the Septic Arthritis entry.

Management is predominantly supportive, since most viral arthritides are self-limiting: NSAIDs (e.g. ibuprofen 400 mg PO tds, or naproxen 500 mg PO bd) for symptomatic relief, with paracetamol as an adjunct or alternative
Parvovirus B19: supportive care as above; specific concern arises in pregnancy (risk of fetal hydrops, see relevant obstetric entries for fetal anemia workup) and in patients with an underlying hemolytic disorder or immunosuppression, where parvovirus can cause a transient aplastic crisis (see Sickle Cell Disease entry) rather than simple arthropathy
Chikungunya: NSAIDs and analgesia for the acute phase; persistent arthralgia beyond 3 months (chronic chikungunya arthropathy) may require a more structured approach akin to inflammatory arthritis management, including consideration of hydroxychloroquine or methotrexate in refractory cases under rheumatology guidance
Hepatitis B or C associated arthritis: managed alongside treatment of the underlying viral hepatitis (see those entries), with the arthritis typically improving as viral load is controlled
Treatment of the specific underlying viral infection follows its own dedicated pathway where one exists and disease-modifying treatment is available and indicated (see Hepatitis B, Hepatitis C, HIV entries)

Referral: rheumatology for persistent symptoms beyond the expected self-limiting course, or diagnostic uncertainty with inflammatory arthritis; obstetrics for parvovirus B19 exposure in pregnancy.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Osteoarthritis

Degenerative joint disease characterized by progressive cartilage loss, subchondral bone remodeling, osteophyte formation, and low-grade synovial inflammation, resulting from an imbalance between cartilage breakdown and repair. Most common form of arthritis, leading cause of disability in older adults.

Risk factors: age, obesity (mechanical load + metabolic/inflammatory contribution), female sex, joint malalignment, previous joint injury/trauma, occupational/repetitive joint loading, genetic predisposition, prior inflammatory arthritis.

Classified by:

Primary (idiopathic): no identifiable underlying cause, associated with aging/wear
Secondary: due to identifiable cause ; post-traumatic, inflammatory arthritis sequelae, metabolic (hemochromatosis, ochronosis), congenital/developmental joint abnormality, avascular necrosis
Commonly affected joints: knees, hips, hands (DIP/PIP joints, first CMC joint), spine (facet joints), first MTP joint

Joint pain: mechanical pattern ; worse with activity/weight-bearing, relieved by rest (distinguishes from inflammatory arthritis where rest worsens/morning stiffness prolonged)
Morning stiffness: typically brief, <30 minutes (contrast with rheumatoid arthritis where morning stiffness >1 hour is characteristic)
Reduced range of motion, crepitus on joint movement
Joint examination findings:
Bony swelling/enlargement (not soft/boggy synovitis as in inflammatory arthritis)
Heberden's nodes (DIP joints), Bouchard's nodes (PIP joints) ; hand OA
Fixed flexion deformity, varus/valgus deformity (knee OA)
Reduced internal rotation (early sign, hip OA)
Mild joint effusion possible but marked warmth/erythema atypical (suggests alternative/superimposed inflammatory process, e.g., crystal arthropathy)
Functional impact: difficulty with stairs, walking distance, rising from chairs, fine motor tasks (hand OA)
Progressive course, though pain severity does not always correlate with radiographic severity

Primarily clinical for typical presentation (age >45, activity-related pain, no/brief morning stiffness); imaging not always required to confirm diagnosis in classic cases (per NICE clinical diagnosis criteria).

Plain radiographs (weight-bearing views for knee/hip): joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts; classic findings but severity doesn't always correlate with symptoms; useful to exclude other pathology or when diagnosis uncertain, or pre-surgical planning
Blood tests: NOT required for diagnosis, generally normal (ESR/CRP normal or mildly elevated) ; used to exclude inflammatory arthritis if diagnostic uncertainty (rheumatoid factor, anti-CCP, ANA if inflammatory features present)
Joint aspiration: if effusion present and diagnostic uncertainty : synovial fluid analysis (non-inflammatory, WCC <2000/mm³ typical in OA) helps exclude septic arthritis, crystal arthropathy (gout, pseudogout)
MRI: not routine, reserved for specific indications (suspected meniscal/ligamentous injury, avascular necrosis, atypical presentation)

Differentials: rheumatoid arthritis and other inflammatory arthropathies (prolonged morning stiffness, symmetric small joint involvement, systemic symptoms, elevated inflammatory markers), gout/pseudogout (acute, monoarticular, marked erythema/warmth), septic arthritis (acute, hot, systemically unwell — exclude urgently if acute monoarticular presentation), avascular necrosis, referred pain (hip OA can present as knee pain).

Core/first-line (all patients):

Patient education: nature of condition, self-management expectations
Weight loss if overweight/obese (significant impact on symptom burden and disease progression, especially weight-bearing joints)
Exercise: strengthening (particularly quadriceps for knee OA) and aerobic exercise ; improves pain and function, does NOT accelerate joint damage (address common patient misconception)
Physiotherapy referral for individualized exercise program, gait aids assessment (cane, walking aids)

Pharmacological (symptom control, does not modify disease progression):

Topical NSAIDs (diclofenac gel); first-line for knee/hand OA, particularly favored in older patients (fewer systemic effects)
Oral NSAIDs: first-line if topical insufficient ; use lowest effective dose, shortest duration, with gastroprotection (PPI co-prescription) if risk factors (age, GI history, concurrent anticoagulant/steroid); caution in cardiovascular disease, renal impairment
Paracetamol: modest efficacy alone per current evidence, may be used as adjunct but no longer considered strongly effective as monotherapy in current guidelines
Topical capsaicin: adjunct option for localized joint pain
Intra-articular corticosteroid injection: short-term symptom relief (weeks-months) for flares, particularly knee OA ; avoid frequent repeated injections (cartilage toxicity concern with excessive use)
Intra-articular hyaluronic acid: evidence mixed/weak, not routinely recommended by major guidelines (e.g., NICE, AAOS) though used in some practice
Duloxetine: option for chronic OA pain, particularly with central sensitization component
Opioids: NOT recommended for routine use given poor risk-benefit in chronic non-cancer pain ; reserved for short-term severe flares awaiting definitive treatment, avoid long-term use

Surgical management (for severe disease refractory to conservative management, significant functional limitation/quality of life impact):

Joint replacement (arthroplasty) ; knee/hip most common, highly effective for pain relief and function restoration
Osteotomy: selected younger patients with malalignment, joint-preserving option
Arthroscopic debridement/meniscectomy: limited role, not recommended for pure OA management (evidence does not support benefit over sham/conservative management in absence of mechanical locking symptoms)

Referral: orthopedics for surgical assessment when conservative management fails and significant functional impairment/pain persists; rheumatology if diagnostic uncertainty or inflammatory features present.

Viral Arthritis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management