Early recognition and intervention is important to prevent joint destruction – prognosis is poorer, the longer it is before detection. Destructive changes to joint can begin to occur within hours.
Pathogenesis:
Synovial membranes are invaded by micro-organism extends into the joint space avascular cartilage is degraded by bacterial and lysosomal enzymes
Inflamed and hypertrophic synovium granulation tissue (pannus) expands
Eventually irreversible loss of joint function.
Routes of infection:
1) Haematogenous spread from remote site (seeding of synovial membrane from direct transport of organisms in the synovial vascular supply) – most common pathogenesis
2) From sepsis in adjacent tissue (intra-articular extension of osteomyelitis)
3) Implantation/direct invasion (eg during aspiration or from a puncture wound)
4) Spread form infection near joint via lymphatics
– also (5) An immunologic process that can be triggered by a remote infection (eg Reiters syndrome)
Predisposing/risk factors:
Infection; age > 80yrs; previous damage to joint (eg osteoarthritis, rheumatoid arthritis, gout, trauma, surgery); joint implant/prosthesis; chronic illness, especially those associated with impaired immunity/defences (eg diabetes mellitus, renal disease, malignancy, HIV); immunosuppressive and corticosteroid therapy.
Clinical features:
Acute onset of pain in joint (80-90% are monoarticular) is classical presentation – minimal movement induces pain; local swelling; tenderness; erythema; warmth; restricted range of motion. Most have fever.
Bacterial infection normally only affects one joint. Viral infection more commonly affects several joints.
X-ray:
Joint swelling (from oedema, effusion and hypertrophy); osteoporosis; loss of joint space (when inflammatory pannus destroys chondral region); marginal and central erosions (from pannus destruction)
Laboratory:
Synovial fluid analysis – culture (and sensitivity), gram stain, white cell count, polarising microscopy (to rule out crystal deposition).
Differential diagnosis – crystal deposition disease; trauma; acute exacerbation of inflammatory disease.
Treatment:
Need to have a high ‘index of suspicion’ for clinical features in those with risk factors.
Early and aggressive treatment is needed to prevent joint destruction.
Initially – repeated daily aspiration/drainage, antibiotics (large IV doses), immobilisation of joint, analgesics
Subsequent – daily monitoring of patients status (temperature, appetite); range of motion exercises; definitive antibiotics; serial joint aspiration; surgical drainage.
Specific Infections:
Gonococcal arthritis:
• usually part of complex associated with disseminated gonococcal infection (DGI) – due to haematogenous spread of Neisseria gonorrhoeae – arthritis occurs in 1-4%
• generally in young, healthy, sexually active individuals
• most common cause of septic arthritis in the sexually active between ages of 15 and 45 years
• polyarthritis is just as common as monoarthritis – knee and ankle most common sites
• present 2 days to 2 months following sexual contact that caused infection
• genitourinary symptoms are frequently absent
• tenosynovitis (often migratory) and skin lesions are common (typically a rash that starts as small, painful pustule with and erythematous base ulcerate during healing)
• treatment – antibiotics (IV initially), joint immobilisation, regular aspiration
Non-gonococcal arthritis:
• most are Staphylococcus aureus (up to 70% in those <14 years and >45 years), but also S. epidermidis (more common in prosthetic joint infections) and Streptococcus (25%); Haemophilus influenzae (more common in children). Less commonly, Pneumococcus (becoming rare), Esherichia coli (more commonly in those who are seriously ill, elderly or IV drug users)
• source of infection is usually a puncture wound, open lesions, adjacent infection (cellulitis, oetomyelitis) or haematogenous spread.
• many follow inadequate treatment of existing infection
Tuberculous arthritis:
• chronic granulomatosis arthritis due to Mycobacterium tuberculosis
• incidence is increasing because of its association with HIV infection.
• 1-3% of those with tuberculous have joint involvement
• typically monoarthritis and combined with osteomyelitis – onset tends to be insidious rather than acute; gradually destruction of joint
• usually hip, knee and ankle
• treatment – antibiotics and joint immobilisation
Fungal/mycotic arthritis:
• rare – more common in immunosuppressed individuals
• usually chronic monoarticular arthritis
• many organisms implicated – coccidioidomycosis, histoplasmosis, blastomycosis, candidiasis, sporotrichosis, cryptococcosis
• diagnosis by culture of from joint fluid or microscopy of fluid or synovial biopsy
• treatment usually with aspiration, debridement and pharmacotherapy (amphotericin B or ketoconazole)
Viral arthritis:
• most commonly rubella, hepatitis B, parvovirus and alphavirus
• virus may directly invade synovium or immune complex may cause reaction in joint
• usually have fever, chills, headache, malaise, muscle aches
• typically arthritis is usually rapid onset, symmetrical and migratory polyarticular involvement of small joints of hands and the knees; morning stiffness – lasts for up to 3 weeks – not as acute as other forms of septic arthritis; non-suppurative
• 10-25% of those with hepatitis B develop joint symptoms
• 30% of female and 6% of males with rubella joint symptoms
• alphavirus infections typically have fever, arthritis and skin rash; arthritis may be severe – affects hands, wrists, elbow, knees and ankles – generally symmetric and polyarticular. Most likely due to, for example, Ross River virus (Australia, NZ, South Pacific); Mayaro virus (South America); Sindbis virus (Europe, Asia, Africa).
• treatment is symptomatic (most self limiting) – analgesics and NSAID’s
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