Septic arthritis

Septic arthritis, also known as infectious arthritis, is a medical condition characterized by the invasion of a joint space by pathogenic microorganisms, most commonly bacteria, leading to inflammation, synovial fluid accumulation, and potential destruction of articular cartilage and bone. Prompt recognition and treatment are essential to prevent irreversible joint damage and systemic complications.

Etiology

• Bacterial agents: Staphylococcus aureus is the most frequent cause in adults, while Streptococcus species, Haemophilus influenzae, and Neisseria gonorrhoeae are also implicated. In neonates and young children, Streptococcus pneumoniae and Group B Streptococcus are notable pathogens.
• Fungal agents: Candida species and Aspergillus spp. may cause septic arthritis, particularly in immunocompromised individuals.
• Mycobacterial agents: Mycobacterium tuberculosis can produce a chronic form of septic arthritis (tuberculous arthritis).

Pathophysiology
Microorganisms reach the joint via hematogenous spread, direct inoculation (e.g., penetrating trauma, surgical procedures), or contiguous extension from adjacent infected tissue. Once within the synovial cavity, bacterial proliferation triggers an intense inflammatory response mediated by neutrophils and cytokines. The resulting enzymatic and oxidative damage to cartilage matrix and subchondral bone can rapidly compromise joint integrity.

Epidemiology

• Incidence varies geographically but is estimated at 2–10 cases per 100,000 population annually in developed nations.
• The condition is more common in males and peaks in two age groups: infants (especially under 3 months) and adults over 60 years.
• Risk factors include pre-existing joint disease (e.g., rheumatoid arthritis, osteoarthritis), immunosuppression, intravenous drug use, prosthetic joints, and recent joint injections.

Clinical Presentation
Typical signs and symptoms include:

• Acute onset of joint pain, often severe and worsening over hours.
• Swelling, warmth, and erythema of the affected joint.
• Restricted range of motion due to pain.
• Systemic features such as fever, chills, and malaise may be present, especially in bacterial infections.

Diagnosis

1. Joint aspiration: Synovial fluid analysis is the cornerstone; findings often show purulent fluid with a high white blood cell count (>50,000 cells/µL) predominantly neutrophils, low glucose, and elevated protein.
2. Microbiological culture: Gram stain and aerobic/anaerobic cultures of synovial fluid identify the causative organism in 60–80 % of cases.
3. Imaging: Plain radiographs may appear normal early; later stages show joint space narrowing and erosions. Ultrasound can detect effusion; MRI is sensitive for soft‑tissue and bone involvement.
4. Laboratory tests: Elevated erythrocyte sedimentation rate (ESR) and C‑reactive protein (CRP) support an inflammatory process but are non‑specific.

Management

• Empiric antimicrobial therapy: Initiated promptly after synovial fluid aspiration, typically covering Staphylococcus aureus (including methicillin‑resistant strains) and Gram‑negative organisms. Regimens are later adjusted based on culture results.
• Joint drainage: Repeated needle aspiration, arthroscopic lavage, or open surgical drainage is employed to remove purulent material and reduce intra‑articular pressure.
• Adjunctive measures: Analgesia, immobilization of the joint for short periods, and physiotherapy after infection control to preserve function.
• Prosthetic joint infection: May require prosthesis removal, staged revision, or long‑term suppressive antibiotics.

Prognosis
Outcomes depend on the speed of diagnosis and adequacy of treatment. Delay beyond 48 hours increases the risk of irreversible cartilage loss, joint deformity, and functional impairment. Mortality rates are low in otherwise healthy individuals but higher in the elderly, immunocompromised, or those with septic shock.

Prevention

• Sterile technique during intra‑articular injections and surgical procedures.
• Prompt treatment of bacteremia and skin infections to reduce hematogenous spread.
• Vaccination against pathogens such as Haemophilus influenzae type b and Streptococcus pneumoniae may indirectly lower risk.

References
(Encyclopedic entries typically cite peer‑reviewed medical textbooks and guidelines; specific citations are omitted here for brevity.)