Septic arthritis Flashcards

1
Q

What are the differential diagnosis of acute monoarthritis?

A

1) Septic arthritis
2) Crystal arthritis: gout, pseudogout, apatite related
3) First presentation of inflammatory arthritis such as rheumatoid arthritis
4) Reactive arthritis
5) Intra- articular injury (fracture, meniscal tear)
6) Hemarthrosis
7) Metastatic carcinoma

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2
Q

What are the risk factors for acquiring septic arthritis?

A

Immunocompromised: >80yo, DM, cirrhosis, HIV, alcoholic

Diseased joint: chronically inflamed (eg RA/OA), prosthetic joints

For haem spread (majority): recent bacteraemia, recent endocarditis, recent skin infection, IVDU, IDC, central/peripheral lines

  • Note: may not have bacteraemia at presentation: presumably transient/self-limited bacteraemia
  • Note: in pt w no RF, w staph/strep/enterococci SA, think endocarditis!!

For direct inoculation: recent acupuncture or bite near joint/joint aspiration/ intra-art GC/ joint surgery/ open skin over joint

For contiguous spread: recent OM

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3
Q

What are the pathogens that cause septic arthritis?

A

Non-gonococcal
• Staph. aureus (>50%), GAS, GBS. Staph A is a very sticky organism and can seed to joints!
•Gram –ve rods (E. coli, Proteus, Klebsiella, Enterobacter)
• H. influenzae in children

Gonococcal (Neisseria gonorrhoea)
• Sexually active groups
• Has a more oligo/polyarticular, migratory pattern, w tenosynovitis and rash
•Blood and Joint Aspirate C/S are usually -ve -> Dx depends on HOPC, Hx + Mucosal swab C/S (urethral / cervical)

Usually monomicrobial (mostly staph), if polymicrobial think

  • Penetrating trauma involving joint space
  • Direct extension from bowel (eg ruptured diverticular) entering post thigh and hip joint via retroperitoneal space
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4
Q

What are the clinical features of septic arthritis?

A

Joint: acute onset monoarthritis - pain, swelling, redness, Inability to WB

  • Usually Pain&raquo_space;> Signs! With severe limitation in ROM
  • Knee (~50%), hip, shoulder, elbow, ankle, Sternoclavicular Joint (esp IVDU)
  • Rapid & Acute Onset, worsening over 3 days (unlike gout which is within 12-24 hrs)
  • Typically Monoarticular (but can be polyarticular, except if DGI)

Systemic: fever (60%) (may not be observed in older pts), toxic and unwell

  • This is not mandatory!
  • Depending on aetiology, infection may be localised within joint and hence no systemic S&S
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5
Q

What are the investigations required for septic arthritis?

A

Joint aspirate: gold standard

  • TWC + differential, Gram stain & c/s, glucose, AFB, polarised microscopy
  • Presence of crystals DOES NOT RULE OUT SEPTIC ARTHRITIS!
  • If fungal / TB suspected: Acid Fast Stain, Mycobacterial PCR & C/S, Fungal stain & C/S
  • cloudy/purulent
  • WBC >50K (>1.1K for prosthetic) diagnostic
  • Glucose <60% serum level: just remember Low Glucose High Protein

Labs

  • FBC: raised WBCs (left shift)
  • Blood c/s
  • CRP: usually >5

XR joint TRO concurrent joint disease / OM

2DE TRO IE if no clear source of infection in pts w known valvular heart disease/ polyarticular involvement

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6
Q

What is the management of septic arthritis?

A

Acute

1) Emp IV abx STAT aft joint aspiration
- Native joint (mostly Staph aureus): IV cefazolin (2nd line: IV cloxacillin, IV genta)
- If Penicillin allergy = Clindamycin
- Prosthetic joint : IV vancomycin – higher chance to be Staph A?
2) Surgical: irrigation and drainage of joint +- debridement

Post-acute

  • Early PT: prevents stiffness, muscle wasting
  • Monitor clinically w FBC, CRP
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7
Q

What is the clinical presentation of gonococcal arthritis?

A

1) RASH
2) SYSTEMIC S&S
3) MIGRATORY POLYARTHRITIS
4) TENOSYNOVITIS

Initial phase

  • Fever and malaise: due to haematological spread of Gonorrhoea
  • **Painless pustules/vesicles on peripheries
  • *Migratory asymmetrical polyarthritis: Commonly affects knees, elbows, ankles, knees
  • **Tenosynovitis: asymmetrical, affecting fingers, wrist, ankles, knees
  • 40% have gonococcemia (+ve blood cultures)

Settling of initial phase

  • Blood cultures become –ve
  • NAATs (nucleic acid amplification tests) are a useful adjunct to cultures

Later phase

  • Large joint monoarthritis or oligoarthritis
  • Culture is usually +ve from genital tract, although joint fluid may be sterile
  • Unclear distinction whether it is a septic arthritis or a response to bacterial LPS
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8
Q

What are the investigations required for gonococcal arthritis?

A

**sexual history

FBC

CRP

Blood c/s, joint aspiration (usually be sterile)

  • +ve jnt aspirate culture only 25-30%
  • +ve blood culture only 40%

Consider c/s of mucosal surfaces to increase yield: oral, urethral, cervical
- +ve culture of mucosal surface swabs (esp site of pri infection) is at 80%!

NAATs – much more sensitive than culture, can be done for Blood/Joint Aspirate/Mucosal Swab when cultures turn out negative!

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9
Q

What is the management of gonococcal arthritis?

A

Screen for concurrent Chlamydia infection (recall, the 2 predisposes each other) + screen for all other STIs

(TTSH) IV Ceftriazone + doxy (also covers for chlamydia). If resistant to ceftriazone: IV azithro

Joint rest

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10
Q

What are the clinical features of tuberculous arthritis?

A
  • Spine (50%; Pott’s Dz) or hip/knee (30%) involvement, may affect mandible or vertebrae
  • Febrile, night sweats, weight loss, anorexia
  • Usual risk factors for TB apply: debility, excess alcohol use, immunosuppression, HIV/AIDs
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11
Q

What are the investigations required for tuberculous arthritis? ?

A
  • Joint fluid c/s, synovium bx and c/s
  • CXR to look for pTB
  • Joint/spinal XR may show joint-space reduction and bone destruction if treatment delayed, but MRI spine detects abnorm earlier
  • CT-guided bx from affected IV disc often needed to obtain c/s
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