Septic Arthritis

Wikis > Rheumatology > Septic Arthritis

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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