Acute Hot Joint Flashcards

1
Q

(2) most common organisms causing septic arthritis

A
  • most common organism overall is Staphylococcus aureus
  • in young adults who are sexually active Neisseria gonorrhoeae should also be considered
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2
Q

The most common location of septic arthritis in adults

A

in adults, the most common location is the knee

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3
Q

Criteria for diagnosis of septic arthritis

A

The Kocher criteria for the diagnosis of septic arthritis:

  • fever >38.5 degrees C
  • non-weight bearing
  • raised ESR
  • raised WCC
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4
Q

Management of septic arthritis

A
  • synovial fluid → obtained before starting treatment
  • IV antibiotics → which cover Gram-positive cocci (flucloxacillin or clindamycin if penicillin allergic)

*antibiotic treatment is normally be given for several weeks (6-12 weeks)

  • needle aspiration → to decompress the joint
  • arthroscopic lavage may be required
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5
Q

Differential diagnosis of acute hot joint

A
  • Septic arthritis (bacterial, mycobacterial ,fungal)
  • Lyme disease
  • Crystal arthritis (gout, pseudo-gout -calcium pyrophosphate deposition disease)
  • Trauma
  • Haemarthrosis (eg haemophilia)
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6
Q

What to ask in Hx of hot joint?

A
  • How quickly did the pain and swelling come on?
  • Are any other joints involved?
  • Do they feel unwell? Fever/sweats? Have systemic symptoms eg urinary, chest?
  • Have they damaged the joint? eg recent intra-articular injection
  • Have they had a recent infection of any kind?
  • Is there a history of IV drug use? (consider infection)
  • Have they had previous episodes of pain and swelling in other joints that resolved spontaneously? (consider crystal arthritis)
  • Do they have a history of arthritis? Gout?
  • Are they immunosuppressed? (diabetes, steroids, DMARDs)
  • Do they have a bleeding diathesis? Anti-coagulated? (consider haemarthrosis)
  • Ask about genito-urinary symptoms and sexual history
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7
Q

What to examine in the patient with an acute hot joint?

A
  • Examine the joint – red, hot and swollen!
  • Examine the other joints – are others involved
  • Signs of arthritis eg OA, RA? Tophi?
  • Systemic examination – skin eg rashes, track marks; chest; heart sounds etc
  • Vital signs – pay particular attention to BP
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8
Q

Is there any fever in septic arthritis?

A

fever – can be misleading: often present in septic arthritis but can be absent.

Can be a feature of acute gout or pseudogout.

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9
Q

Ix for septic arthritis

A
  • FBC, U+E
  • CRP or ESR (useful for monitoring response to treatment)
  • Blood cultures x 2
  • JOINT ASPIRATION → synovial fluid analysis is the single most useful diagnostic test for a hot joint
  • Request cell count, gram stain, culture, crystal examination
  • Consider imaging eg baseline Xray, ultrasound to guide joint aspiration
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10
Q

Ranges of synovial fluid WCC

A

Synovial fluid white cell count:

< 500/mm3 → non-inflammatory fluid

> 1500/mm3 → inflammatory fluid

> 50,000/mm3 → think of septic arthritis

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11
Q

How bacteria reach the joint in septic arthritis?

A
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12
Q

Risk factors for the development of septic arthritis

A

Abnormal/damaged joint

  • Pre-existing arthritis eg RA, OA
  • Prosthetic joints

Impaired host defense

  • Elderly (>65y), children (<5y)
  • Chronic illness eg diabetes, liver cirrhosis, chronic renal disease, alcoholism, cancer
  • Immunosuppressed eg steroids, chemotherapy, hypogammaglobulinaemia, HIV
  • Intravenous drug abuse
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13
Q

Antibiotic choice in septic arthritis

A
  • No risk factors for atypicals → cover staph and strep: flucloxacillin + penicillin
  • High risk of gram negative sepsis → 2nd/3rd generation cephalosporin eg cefuroxime
  • MRSA risk, eg nursing home resident, leg ulcers → vancomycin
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14
Q

Length of treatment with antibiotics in septic arthritis

A

IV antibiotics for 2/52 then orally for 4/52

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15
Q

Other (than antibiotic and aspiration) notes on the management of septic arthritis

A
  • Analgesia
  • Drain the joint to dryness regularly eg repeated joint aspiration
  • Immobilise the joint for a day or 2, then gentle physical therapy
  • Treat the focus of infection and manage sepsis eg IV fluids
  • DVT prophylaxis
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16
Q

What’s gout?

A

Gout is a form of microcrystal synovitis (inflammation) caused by the deposition of monosodium urate monohydrate in the synovium.

It is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l)

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17
Q

Risk factors for the development of gout

A

Decreased excretion of uric acid

  • drugs: diuretics, aspirin 75-150 mg (but continue if CVD)
  • chronic kidney disease
  • lead toxicity

Increased production of uric acid

  • myeloproliferative/lymphoproliferative disorder
  • cytotoxic drugs
  • severe psoriasis
  • excess dietary purine consumption
  • alcohol
  • tumour lysis
18
Q

Which syndrome predisposes to gout?

A

Lesch-Nyhan syndrome

  • hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
  • x-linked recessive therefore only seen in boys
  • features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
19
Q

Symptoms of gout

A

Patients typically have episodes lasting several days when their gout flares and are often symptom-free between episodes

The acute episodes typically develop maximal intensity with 12 hours/ The main features it presents with are:

  • pain: this is often very significant
  • swelling
  • erythema
20
Q

Which joints are affected by gout?

A

Around 70% of first presentations affect the 1st metatarsophalangeal (MTP) joint.

Other commonly affected joints include:

  • ankle
  • wrist
  • knee
21
Q

Radiological features of gout

A
  • joint effusion
  • well-defined ‘punched-out’ erosions with sclerotic margins ina juxta-articular distribution, often with overhanging edges
  • relative preservation of joint space until late disease
  • eccentric erosions
  • no periarticular osteopenia (in contrast to rheumatoid arthritis)
  • soft tissue tophi may be seen
22
Q

Acute management of Gout

A

Acute management

  • NSAIDs or colchicine are first-line

*the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled. Gastroprotection (e.g. a proton pump inhibitor) may also be indicated

*colchicine has a slower onset of action.

The main side-effect is diarrhoea

  • oral steroids may be considered if NSAIDs and colchicine are contraindicated. A dose of prednisolone 15mg/day is usually used
  • another option is intra-articular steroid injection
  • if the patient is already taking allopurinol it should be continued
23
Q

Indications for allopurinol

A

Indications for urate-lowering therapy (ULT)

  • offer urate-lowering therapy to all patients after their first attack of gout

ULT is particularly recommended if:

  • → >= 2 attacks in 12 months
  • → tophi
  • → renal disease
  • → uric acid renal stones
  • → prophylaxis if on cytotoxics or diuretics
24
Q

Lifestyle modification for gout

A
  • reduce alcohol intake and avoid during an acute attack
  • lose weight if obese
  • avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
25
Q

(3) drugs consideration in patient with gout

A
  • consideration should be given to stopping precipitating drugs (such as thiazides)
  • losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
  • increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
26
Q

Synovial fluid microscopy in gout

A
27
Q

What’s an alternative to allopurinol for long-term prophylaxis of gout?

A

febuxostat →another xanthine inhibitor

28
Q

What’s pseudogout?

A

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

29
Q

Risk factors for pseudogout

A
  • haemochromatosis
  • hyperparathyroidism
  • acromegaly
  • low magnesium, low phosphate
  • Wilson’s disease
30
Q

What joints are most commonly affected in pseudogout?

A
  • knee
  • wrist
  • shoulders
31
Q

What’s seen on joint aspiration in pseudogout?

A

weakly-positively birefringent rhomboid-shaped crystals

32
Q

What can be seen on x-ray in pseudogout?

A

chondrocalcinosis

  • in the knee this can be seen as linear calcifications of the meniscus and articular cartilage
33
Q

Management of pseudogout

A
  • aspiration of joint fluid, to exclude septic arthritis
  • NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
  • no prophylaxis available
34
Q

What’s reactive arthritis?

A

Reactive arthritis is defined as an arthritis that develops following an infection where the organism cannot be recovered from the joint

35
Q

Associations with reactive arthritis

A

Reactive arthritis:

  • is one of the HLA-B27 associated seronegative spondyloarthropathies
36
Q

What’s Reiter’s syndrome?

A
  • classic triad of urethritis, conjunctivitis and arthritis → following a dysenteric illness during the Second World War
  • Later studies identified patients who developed symptoms following a sexually transmitted infection (post-STI, now sometimes referred to as sexually acquired reactive arthritis, SARA)
37
Q

What are the organisms causing reactive arthritis?

A
  • Urogenital eg Chlamydia trachomatis
  • Enterogenic eg salmonella, shigella, campylobacter, Yersinia
  • Others eg Chlamydia pneumoniae, Clostridium dificile, Streptococcus
38
Q

Demographics of reactive arthritis

A
  • Primarily affects young adults 20-40y
  • Enterogenic → male=female
  • Urogenic → predominantly male
39
Q

How long does reactive arthritis last?

A
  • Usually develops within 1-4w of infection
  • Remission of symptoms in most patients within 6 months
40
Q

Management of reactive arthritis

A
  • Treat the triggering infection if indicated eg chlamydia

Articular disease:

  • NSAIDs
  • Intra-articular steroids
  • Oral steroids

Persistent/refractive disease:

​- DMARDs eg sulphasalazine