Septic, Crystal and Reactive Arthritis Flashcards

1
Q

What are the causes of acute monoarthritis?

A
  • infection
  • crystal (gout, calcium pyrophosphate)
  • reactive (inflammation)
  • haemoarthrosis (bleeding into joint)
  • systemic rheumatic condition
  • trauma
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2
Q

Describe the clinical features of acute monoarthritis

A
  • inflammation signs (redness, heat, discomfort, swelling)
  • +/- fever (can be dampened if patient is on certain drugs)
  • +/- leucocytosis, raised CRP (can be blunted)
  • be aware of atypical presentations
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3
Q

What is the most important thing to remember about acute monoarthritis?

A

acute monoarthritis is septic until proven otherwise (negative aspirate)

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4
Q

What are the risk factors for septic arthritis?

A
  • previous arthritis
  • trauma
  • diabetes mellitus (esp if poorly controlled)
  • immunosuppression
  • bacteraemia (eg. self-catheterising/changing catheters)
  • sickle cell anaemia
  • prosthetic joint
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5
Q

Describe the pathogenesis of septic arthritis

A
  • bacteria enter joint and deposit in synovial lining
  • most common by haematogenous spread (can also by local invasion/ inoculation)
  • rapid entry into synovial fluid (due to limited host response)
  • good environment for pathogen due to lack of basement membrane and close relationship to blood vessels
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6
Q

Describe the features of septic arthritis

A
  • > 60
  • on average 4 joints (knee, elbow, shoulder and hip)
  • commonly RA (without fever or leucocytosis)
  • blood/synovial fluid culture (both effective)
  • staph and strep most common pathogens
  • poor prognosis (1/3 mortality)
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7
Q

What is the management for septic arthritis?

A
  • joint aspiration (to reduce burden and washout joint)
  • antibiotic therapy
  • surgical intervention (if not responding after 48hrs of therapy - consult orthopaedics)
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8
Q

List the risk factors for gout

A

Non-modifiable: age, male, race, genetic factors, impaired renal function

Modifiable: obesity, alcohol, high-purine diet (meat and seafood), fructose corn syrup, medications

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9
Q

What medications can put you at risk for gout?

A
  • aspirin (reduces UA excretion which can lead to progressive accumulation)
  • diuretics
  • cyclosporin
  • pyrazinamide and ethambutol
  • nicotinic acid
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10
Q

When can a diagnosis of gout be made on clinical suspicion?

A
  • typical presentation of podagra
  • history of gout flares or hyperuricaemia
  • raised sUA between attacks
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11
Q

What differentials should you keep in mind when considering a diagnosis of gout?

A
  • septic arthritis
  • CPPD
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12
Q

What are the goals of gout treatment?

A

Acute attacks: relieve pain and reduce inflammation
- cold-packs, NSAIDs/colchicine/corticosteroids

Long-term: prevent attacks and joint damage and eliminate top (crystals)

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13
Q

List the urate lowering therapies

A
  • allopurinol (100mg then increase every 4w until target)
  • febuxostat (80mg, can go to 120mg in 4w if not target)
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14
Q

What are the important features of reactive arthritis?

A
  • serum-negative for rheumatoid factor
  • associated with HLA-B27
  • tends to develop soon after an infection
  • no viable organism (not septic arthritis)
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15
Q

Describe the clinical features of reactive arthritis

A
  • acute (2-6 weeks post infection)
  • warm, swollen, tender joints (commonly lower limb)
  • systemically unwell (inflammatory markers raised + malaise)
  • arthritis, conjunctivitis and urethritis
  • most will resolve but can recur
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16
Q

List the common pathogens which cause infective arthritis

A
  • staph and strep (healthy persons)
  • aerobic gram negative bacteria, mycobacteria and fungi (immune-compromised host)
17
Q

What are some signs that can be seen at the affected joint in reactive arthritis?

A
  • lower limb asymmetric oligoarthritis
  • dactylitis (sausage digits)
  • enthesopathy (tendon inflammation)
  • inflammatory back pain
18
Q

What are some extra-articular features of reactive arthritis?

A
  • conjunctivitis, iritis, keratitis, episcleritis
  • keratoderma blennorhagica, nail dystrophy
  • circinate balanitis
  • stomatitis, diarrhoea
  • aortitis (rare)
19
Q

What are the proposed mechanisms of pathogenesis of reactive arthritis?

A
  • cross reactivity between a bacterial antigen and joint tissues resulting in a perpetuated Th2 cell mediated response

or

  • persistence of antigenic material (heat shock proteins) due to a failed clearance possibly due to polymorphism of toll-like receptors
20
Q

How would you investigate reactive arthritis?

A
  • joint aspirate (exclude sepsis)
  • swabs (urethral/cervical - SARA)
  • screen for other related infections
  • ESR/CRP
  • chlamydia serology
  • HLA-B27 serology
21
Q

Describe the management for reactive arthritis

A
  • mild disease: NSAID + simple analgesia
  • moderate disease: joint aspirate + NSAID + corticosteroid injection
  • severe or prolonged disease: refer to rheumatology and consider DMARD