Septic Arthritis

Septic arthritis is direct microbial invasion of the synovial joint space producing a purulent effusion. It is a true orthopaedic emergency—articular cartilage can be irreversibly destroyed within 24–48 hours by bacterial enzymes and the host inflammatory response, so it demands immediate aspiration and treatment without waiting for cultures.

Definition & classification

Septic (suppurative/pyogenic) arthritis is infection of a native or prosthetic joint by pyogenic organisms, leading to inflammatory destruction of cartilage and bone. It is distinguished from reactive arthritis (sterile, post-infectious) and from osteomyelitis (bone infection), though the two coexist in children where the metaphysis is intra-articular.

Classification by route of infection:

Route	Mechanism	Typical setting
Haematogenous	Bacteraemia seeds synovium (most common)	Children, IV drug users, immunosuppressed
Contiguous spread	From adjacent osteomyelitis / soft tissue	Neonates (metaphysis intra-articular), diabetic foot
Direct inoculation	Trauma, surgery, intra-articular injection, bites	Iatrogenic, animal/human bites

By host/joint:

• Native-joint septic arthritis vs prosthetic-joint infection (PJI).
• Monoarticular (~80–90%) vs polyarticular (suggests gonococcal, rheumatoid, or sepsis).
• Gonococcal vs non-gonococcal—a clinically and prognostically distinct split.

High-yield: The knee is the most commonly affected joint in adults (~50%), followed by hip. In infants/neonates the hip predominates. The hip and shoulder lack a protective bony rim, so infection can rapidly compromise the blood supply (femoral head AVN).

Etiology & microbiology

Staphylococcus aureus is the single most common organism overall in native joints across all age groups beyond the neonatal period. The organism depends heavily on age, sexual activity, and host factors.

Group	Most likely organism(s)
Adults (overall)	Staphylococcus aureus
Sexually active young adults	Neisseria gonorrhoeae (most common in this group)
Neonates (<3 months)	S. aureus, Group B Streptococcus, Gram-negative bacilli
Children 6 months–5 yrs	S. aureus; Kingella kingae (increasingly recognised), H. influenzae if unvaccinated
Sickle cell disease	Salmonella (and S. aureus) — classic for osteomyelitis/arthritis
IV drug users	S. aureus, Pseudomonas aeruginosa (axial joints—sternoclavicular, sacroiliac)
Prosthetic joint (early)	S. aureus; (late/indolent) coagulase-negative Staph, Cutibacterium
Animal bite (cat/dog)	Pasteurella multocida
Human bite	Eikenella corrodens
Rose-thorn / soil injury	Sporothrix schenckii (chronic monoarthritis)

High-yield: In a sexually active young adult with migratory polyarthralgia, tenosynovitis and a vesiculopustular rash, think disseminated gonococcal infection. Salmonella septic arthritis/osteomyelitis is the classic association with sickle cell disease.

Pathophysiology

Bacteria reach the synovium (richly vascular, no limiting basement membrane) via blood or direct inoculation. Within the closed joint space they multiply and trigger a brisk acute inflammatory response.

Sequence of cartilage destruction:

1. Bacterial proliferation → release of endotoxins/exotoxins.
2. Neutrophil influx → release of proteolytic enzymes (matrix metalloproteinases, elastase) and reactive oxygen species.
3. Degradation of proteoglycan first, then collagen of articular cartilage—proteoglycan loss is detectable within 8 hours.
4. Rising intra-articular pressure + enzymatic damage → cartilage necrosis, chondrolysis.
5. In the hip/shoulder, pressure tamponade of vessels → avascular necrosis (AVN) of the femoral/humeral head.

Flow of damage: Bacterial seeding → synovitis & purulent effusion → proteoglycan loss (hours) → collagen/cartilage destruction → subchondral bone erosion & AVN → fibrous/bony ankylosis.

High-yield: Cartilage destruction begins within hours and is essentially irreversible after 24–48 hours—this is why septic arthritis is a surgical emergency and aspiration must not be delayed.

Clinical features

The classic presentation is an acutely hot, swollen, exquisitely painful joint with markedly restricted active and passive movement, plus systemic features (fever, malaise).

• Single hot, swollen, red joint—the patient resists any movement.
• The joint is held in the position of maximum capsular volume to minimise pain: hip in flexion, abduction and external rotation; knee in slight flexion.
• Systemic: fever, rigors, tachycardia (may be absent/blunted in neonates, elderly, immunosuppressed).
• Pseudoparalysis in neonates/infants—refusal to move the limb, irritability on handling, refusal to bear weight; fever may be absent.
• Hip septic arthritis in a child—refusal to weight-bear, limp, holds hip flexed/externally rotated.

Gonococcal (arthritis–dermatitis syndrome) vs non-gonococcal:

Feature	Gonococcal	Non-gonococcal
Host	Young, healthy, sexually active	Older, comorbid (DM, RA, prosthesis)
Pattern	Migratory polyarthralgia, then mono/oligoarthritis	Monoarticular (large joint)
Tenosynovitis	Characteristic (dorsum of hands/feet)	Uncommon
Skin lesions	Vesiculopustular/haemorrhagic	Absent
Blood cultures	Often negative	Often positive
Synovial culture yield	Low (<50%)	High (>90% if untreated)
Outcome	Excellent, responds rapidly	Higher morbidity, joint damage

High-yield: A child who can bear weight, even with a limp, is unlikely to have hip septic arthritis—non-weight-bearing is one of the four Kocher criteria.

Diagnosis & investigation of choice

Arthrocentesis (joint aspiration) with synovial fluid analysis is the single most important investigation—it must be done before starting antibiotics whenever feasible. Send fluid for cell count + differential, Gram stain, culture & sensitivity, and crystal analysis (to exclude gout/pseudogout).

Synovial fluid interpretation:

Parameter	Normal	Inflammatory (e.g. RA)	Septic
Appearance	Clear, viscous	Cloudy yellow	Purulent/opaque
WBC/mm³	<200	2,000–50,000	>50,000 (often >1,00,000)
% PMN (neutrophils)	<25%	>50%	>75%
Gram stain positive	—	—	~50–70%
Glucose	≈ serum	Low	Very low

High-yield: Synovial WBC >50,000/mm³ with >75% polymorphs strongly suggests sepsis; >1,00,000 is highly specific. No cut-off is absolute—crystals AND infection can coexist, and prosthetic-joint infection presents with much lower counts (WBC >1,100 with >64% PMN is suggestive for PJI).

Supporting investigations:

• Blood cultures (positive in ~50%, higher in S. aureus)—always send before antibiotics.
• ESR & CRP raised; CRP is the most useful for monitoring response (falls faster than ESR). WBC count.
• Procalcitonin may help; serum urate is unreliable in acute attacks.
• Gonococcal work-up: culture/NAAT from urethra, cervix, rectum, pharynx (higher yield than joint fluid).
• X-ray: early normal or shows soft-tissue swelling/effusion; later joint space loss, juxta-articular osteopenia, erosions. Useful to exclude osteomyelitis/fracture.
• Ultrasound: detects effusion (esp. hip, where it guides aspiration); first line in children.
• MRI: most sensitive for effusion, adjacent osteomyelitis, and abscess.

Kocher criteria (paediatric hip)

Used to differentiate septic arthritis of the hip from transient synovitis in children. Four predictors:

1. Non-weight-bearing on the affected side
2. ESR > 40 mm/hr
3. Fever > 38.5 °C (temperature)
4. Serum WBC > 12,000/mm³

Probability of septic arthritis by number of predictors:

Predictors present	Probability
0	<0.2%
1	3%
2	40%
3	93%
4	99%

Many add CRP > 20 mg/L as a fifth, highly significant predictor.

High-yield: Memorise the Kocher predictors with "FEW Now" → Fever >38.5, ESR >40, WBC >12,000, Non-weight-bearing. Three or four positives → presume septic arthritis and aspirate.

Management & drug of choice

Treatment rests on three pillars: (1) drainage of pus, (2) appropriate IV antibiotics, and (3) joint rest/rehabilitation. Drainage + antibiotics together are essential—antibiotics alone cannot sterilise a pus-filled closed space.

Stepwise approach: Suspect → aspirate joint + take blood cultures → start empirical IV antibiotics → urgent surgical drainage/washout (especially hip & shoulder) → de-escalate to culture-directed therapy → splint then early mobilisation.

Empirical antibiotic choice (cover S. aureus):

• Flucloxacillin/cloxacillin (or first-generation cephalosporin like cefazolin) is the empirical drug of choice for suspected staphylococcal/streptococcal disease.
• Add/Use Vancomycin if MRSA is suspected (high local prevalence, prosthesis, IVDU, known carrier).
• Ceftriaxone is the drug of choice for gonococcal arthritis (dramatic response, often without surgery).
• Cover Gram-negatives (e.g. third-gen cephalosporin ± aminoglycoside) in neonates, elderly, immunosuppressed, IVDU.
• Pasteurella (bites) → amoxicillin–clavulanate.

Duration & route: Conventionally IV for ~2 weeks then oral for total 3–4 weeks (non-gonococcal); gonococcal arthritis needs much less (often 7–14 days). Longer for S. aureus, Gram-negatives, or coexisting osteomyelitis.

Drainage options:

• Repeated needle aspiration for accessible joints (knee) responding well.
• Arthroscopic washout—preferred for knee, shoulder.
• Open arthrotomy (surgical drainage)—mandatory and urgent for the hip, especially in children, because the hip cannot be reliably decompressed by needle and AVN risk is high; also for thick loculated pus or poor response.

Prosthetic joint infection: requires surgical strategy—DAIR (Debridement, Antibiotics, Implant Retention) for early/acute infection with stable implant, or one-/two-stage exchange arthroplasty for chronic infection, plus prolonged (often 6–12 week) culture-directed antibiotics including agents active on biofilm (e.g. rifampicin for staphylococci).

High-yield: Septic arthritis of the hip = surgical emergency requiring open drainage/arthrotomy, not just aspiration. Empirical antibiotics are given after aspiration but should never be delayed beyond it. Cloxacillin/flucloxacillin is the antibiotic of choice for community S. aureus; vancomycin for MRSA; ceftriaxone for gonococcus.

Complications

• Articular cartilage destruction → secondary osteoarthritis (commonest long-term sequela).
• Avascular necrosis of femoral/humeral head (pressure + vascular compromise).
• Osteomyelitis of adjacent bone.
• Growth disturbance in children—damage to physis/epiphysis → limb-length discrepancy, deformity (e.g. coxa magna, dislocation/Tom Smith arthritis in neonatal hip sepsis).
• Ankylosis (fibrous or bony fusion), chronic pain, joint instability/dislocation.
• Sepsis, septic shock, death—mortality 10–15% (higher with polyarticular disease, S. aureus, comorbidity).

High-yield: Tom Smith arthritis—destruction/dislocation of the hip following neonatal septic arthritis, presenting later as a painless dislocated hip with limb shortening.

Key differentials

Condition	Distinguishing pointers
Transient synovitis (irritable hip)	Child, afebrile/low fever, can weight-bear, normal/mildly raised inflammatory markers, low Kocher score; self-limiting
Crystal arthropathy (gout/pseudogout)	Sudden monoarthritis; synovial crystals (negatively birefringent needles—urate; positively birefringent rhomboids—CPPD); can coexist with infection
Reactive arthritis	Sterile; 1–4 weeks after GI/GU infection; HLA-B27; "can't see, can't pee, can't climb a tree"
Acute rheumatoid/seronegative flare	Polyarticular, symmetric, known disease; lower synovial WBC
Haemarthrosis / trauma	History of injury/anticoagulation; bloody aspirate
Acute osteomyelitis	Bony (metaphyseal) tenderness, often coexists in children
Lyme arthritis	Endemic exposure, large joint, Borrelia serology

High-yield: Crystals on microscopy do NOT exclude infection. When in doubt, treat as septic until cultures return—the cost of missing sepsis (joint destruction) outweighs over-treatment.

Recently asked / exam angle

• Most common organism in septic arthritis = S. aureus; in sexually active adults = N. gonorrhoeae; in sickle cell = Salmonella; in IV drug users (axial joints) = Pseudomonas.
• Kocher criteria—name the four predictors and recall that ≥3 positive = high probability of hip septic arthritis (image-based "child refusing to bear weight" vignettes are common).
• Synovial fluid cut-offs—WBC >50,000 with >75% PMN; the value tested most often.
• Investigation of choice = joint aspiration before antibiotics.
• Hip septic arthritis management = urgent open arthrotomy/drainage (single-best-answer favourite).
• Most commonly involved joint = knee (adults), hip (neonates/children).
• Tom Smith arthritis and AVN of femoral head as complications.
• Recognising disseminated gonococcal infection (tenosynovitis + dermatitis + migratory arthralgia) and that ceftriaxone is the answer.
• Why septic arthritis is an emergency: proteoglycan loss within 8 hours, irreversible cartilage damage by 24–48 hours.

Rapid revision

1. S. aureus is the commonest cause overall; N. gonorrhoeae in sexually active young adults.
2. Knee = commonest joint in adults; hip = commonest in neonates/children.
3. Joint aspiration before antibiotics is the investigation of choice.
4. Septic synovial fluid: WBC >50,000/mm³, >75% neutrophils, purulent, low glucose.
5. Kocher criteria (FEW-Now): Fever >38.5 °C, ESR >40, WBC >12,000, Non-weight-bearing; ≥3 → presume sepsis.
6. Cartilage damage begins in hours, irreversible by 24–48 h → surgical emergency.
7. Empirical antibiotic of choice = cloxacillin/flucloxacillin (cefazolin); vancomycin if MRSA suspected.
8. Ceftriaxone is the drug of choice for gonococcal arthritis—often resolves without surgery.
9. Hip septic arthritis needs urgent open arthrotomy, not just needle aspiration.
10. Salmonella → sickle cell; Pseudomonas → IVDU (sternoclavicular/SI joints); Pasteurella → cat/dog bite; Kingella kingae → young children.
11. Complications: cartilage loss → OA, AVN, growth arrest, Tom Smith arthritis, ankylosis, sepsis.
12. Crystals do not exclude infection—when in doubt, treat as septic.