Rheumatology + Orthopaedics Flashcards
(743 cards)
Clinical presentation of septic arthritis
Signs + symptoms
- Painful, hot, red, swollen joint - usually single joint
- Restricted movement/stiffness
- Rapid onset
- Systemic symptoms (not always) - fever, malaise, sweats, rigors
Which joints are most commonly affected by septic arthritis?
Hip and knee
What percentage of septic arthritis is polyarticular?
20%
List risk factors for septic arthritis
- Disease of joint e.g. osteoarthritis
- Prosthetic joint
- Recent joint surgery
- Leg ulceration
- Trauma to joint/skin
- IVDU
- Immunosuppression
Describe the possible routes of infection in septic arthritis and give examples of each
- Direct inoculation e.g. joint surgery
- Contigious spread from adjacent bone e.g. osteomyelitis
- Haematogenous seeding from a distant site e.g. bacteraemia due to meningitis
What is the most common causative organism of septic arthritis? List other common causes of septic arthritis
- Staphylococcus aureus most common
- Neisseria gonorrhoea in sexually active
- Group A strep - strep pyogenes most common
- Haemophilus influenza
- E. Coli
Differential diagnosis of acute monoarthritis
- Septic arthritis
- Crystal arthritis - gout or pseudogout
- Reactive arthritis
- Seronegative arthritis
- Haemarthrosis
- Specific to site e.g. knee - bursitis
How can differential diagnosis for acute monoarthritis be narrowed down using a patient’s history?
- Septic arthritis - usually rapid onset, Hx orthopaedic interventions, primary joint disease, IVDU, immunosuppression, sexual history (gonococcal)
- Reactive arthritis - asymmetrical and polyarticular, symptoms of urethritis, conjunctivitis, diarrhoea, rash, travel history (traveller’s diarrhoea)
- Crystal deposition - rapid onset, previous episodes acute attack in same or other joint with spontaneous resolution, use of diuretics, history of renal calculi, alcoholism, presence of tophi, foot joints involved (gout)
- Ankylosing spondylitis - eye inflammation, low back pain
- Psoriatic arthritis - polyarticular, skin/nail symptoms - patches, pitting
- Haemarthrosis - coagulopathy, anticoagulant medications, trauma
Important points in clinical examination of acute monoarthritis
- Affected joint and joints above and below - ROM, soft tissue around joint, effusion
- Skin
- Eyes
- Systemic symptoms - observations, relevant systems e.g. eyes, skin
Which investigations should be used in acute monoarthritis?
+ interpretation
**Joint arthrocentesis for synovial fluid aspiration in any hot, swollen, tender joint with restricted movement. **
(Considered septic arthritis until proven otherwise)
* Send for - WCC, crystal analysis, gram staining, culture
Bloods
* FBC - WCC (infection), Hb (haemarthrosis)
* ESR, CRP - infection, inflammatory/autoimmune
* Blood culture - infection, done even if apyrexial
* Serum urate - gout
* ANA and RF - rheumatoid arthritis, other inflammatory causes
* U&Es - baseline (e.g. prior to antibiotics), may be deranged in sepsis
* LFTs - baseline
Imaging
* Plain X-ray films of affected joint as baseline
* US for diagnosis/guiding aspiration
* MRI if osteomyelitis suspected or deep joint
Bedside
* MSSU, urinalysis
* Wound swab
* Sputum
How should joint arthrocentesis be carried out in acute monoarthritis?
- Refer to orthopaedics if joint prosthesis or hip joint (will require US guidance)
- Should be carried out in sterile environment
- Use smallest needle possible
- Can be done in patients on anticoagulants e.g. warfarin
- Withdraw as much fluid as possible for symptomatic relief, may need to massage joint to encourage drainage
- Cellulitis of skin over joint is relative contraindication
Features of synovial fluid analysis which suggest septic arthritis
- Colour - yellow/green
- Clarity - cloudy/opaque
- Increased viscosity
- WCC > 50,000 cells/mm3
- > 75% neutrophils
- Gram stain positive
- Negative crystals
Features of synovial fluid analysis which suggest a non-inflammatory pathology
- Colour - straw/yellow
- Clarity - translucent
- High viscosity
- WCC - 200-2000 cells/mm3
- <25% neutrophils
- Gram stain negative
- Negative crystals
Features of synovial fluid analysis which suggest inflammatory cause of arthritis
- Colour - yellow
- Clarity - cloudy
- Viscosity - decreased
- WCC - 2000-50000 cells/mm3
- > 50% neutrophils
- Gram stain negative
- Crystals positive
Features of synovial fluid analysis which suggest haemarthrosis
- Colour - red/xanthochromic
- Bloody
- WCC - 200-2000mm3
- 50-75% neutrophils
- Gram stain negative
- Crystals negative
Classification system for septic arthritis
Newman’s class
A - isolation of pathogenic organism from joint
B - isolation of pathogenic organism from another source
C - typical clinical features and turbid joint fluid in presence of previous antibiotic use
D - suggestive pathology or post-mortem features of septic arthritis
Risk factors for gout
- Male gender
- Obesity
- High purine diet - meat and seafood
- Alcohol
- Diuretics
- CVD or CKD
- Family history
Which joints are typically affected by gout?
- Metarsophalangeal joint (base of big toe)
- Carpal joints
- Carpometacarpal joints (base of thumb)
Describe the crystals seen in gout
Negatively birefringent of polarised light
Monosodium urate crystals
Needle shaped
X-ray findings in gout
- Joint space maintained usually
- Lytic lesions in bone
- Punched out erosions - sclerotic borders, overhanging edges
Management of acute gout flare
- NSAIDs first line (+ PPI)
- Colchicine second line if NSAIDs contraindicated e.g. renal impairment, significant heart disease
- Steroids considered third line
Common side effects of colchicine and how to prevent
GI upset - diarrhoea
Lower dose
Describe long-term management of gout
Lifestyle - healthy diet, avoid alcohol, maintain healthy weight
Urate-lowering therapy - started 2-4 weeks after acute flare has settled
* Offerred if multiple/troublesome flares, CKD 3-5, diuretic therapy, tophi, chronic gouty arthritis
* Monitor serum urate levels - aim for <360 micromol/L or lower if tophi/arthritis, frequent flares despite urate below target
* Allopurinol or febuxostat first line (allopurinol in CVD)
Mechanism of action of allopurinol in gout treatment
Xanthine oxidase inhibitor - reduces production of uric acid (product of purine metabolism)