Crystal Arthritis Flashcards
What is gout?
- acute monoarthropathy w/ severe joint inflammation
- >50% occur at metatarsopharyngeal joint of big toe (podagra)
- other common joints = ankle / foot / small joints of the hand / wrist / elbow / knee
- caused by deposition of monosodium urate crystals in + near joints
- attacks may be precipitated by trauma, surgery, starvation, infection or diuretics
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l). It results from either reduced urate excretion (90%) or excess urate production (10%).
What are the risk factors for each?
Reduced Urate excretion (90%):
- Elderly
- Men
- Post-menopausal females
- Impaired renal fxn
- Hypertension
- Diuretics (thiazide + loop)
- Lead toxicity
XS Urate production (10%):
- Dietary (alcohol, sweeteners, red meat, sea food)
- Genetic disorders
- Myelo + lympho proliferative disorders
- Drugs (alcohol, warfarin, cytotoxics)
- Severe psoriasis
What are the clinical features of gout?
- Significant pain
- Swelling
- Erythema
- Episodes last several days + symptom-free in-between episodes
- Acute episodes develop maximal intensity within 12hrs
70% of first presentations affect 1st MTP joint (big toe). Attacks of gout affecting this area were historically called podagra. Other commonly affected joints include the ankle, wrist + knee.
What investigations are done for gout?
- Arthrocentesis w/ synovial fluid analysis → Needle shaped monosodium urate crystals, displaying Negatively birefringence under polarised light
- Serum urate → usually raised but may be normal
- Radiographs → only soft tissue swelling in early stages; later, well defined ‘punched-out’ erosions are seen in juxta-articular bone
What are the radiological features of gout?
- joint effusion an early sign
- well-defined ‘punched-out’ erosions w/ sclerotic margins in a 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
What does this image show?
- XR of pt with gout affecting his feet
- demonstrates juxta-articular erosive changes around 1st MTP joint
- overhanging edges
- associated with moderate soft tissue swelling
- joint space maintained
What does this image show?
- XR of pt with gout affecting hands
- multiple periarticular erosions bilaterally
- adjacent large soft tissue masses
- relatively preserved joint spaces
- in right hand, these findings most prominent at 1st interphalangeal, 2nd-4th PIP, 1st-3rd MCP and CMC joints
- in left hand, findings most prominent at ulnar styloid, scaphulunate joint, 1st + 5th CMC joints, 2nd + 5th MCP joints and 1st interphalangeal joint
What is the management of acute gout?
- NSAIDs or colchicine (1st line)
- maximum dose of NSAID prescribed until 1-2 days after symptoms have settled
- gastroprotection (eg PPI) may also be prescribed
- colchicine has slower onset of action (SE=diarrhoea)
- oral steroids may be considered if NSAIDs + colchicine contraindicated
- another option: intra-articular steroid injection
- if pt already taking allopurinol, it should be continued
The British Society of Rheumatology Guidelines now advocate offering urate-lowering therapy to all patients after their first attack of gout. It is particularly recommended if: there have been more than 2 attacks in 12 months, tophi present, renal disease, uric acid renal stones or prophylaxis if on cytotoxics or diuretics.
What is the urate-lowering therapy drug?
- 1st line → allopurinol
- delay starting allopurinol until 2 weeks after acute attack
- initial dose of 100 mg od, dose titrated every few weeks to aim for serum uric acid of <300 umol/l
- lower initial dose given if pt has reduced eGFR
- colchicine (or NSAID) cover considered when starting allopurinol
- 2nd line → febuxostat
What lifestyle/other advice should be given for gout?
- reduce alcohol intake + avoid during an acute attack
- lose weight if obese
- avoid food high in purines eg. liver, kidneys, seafood, oily fish (mackerel, sardines) + yeast products
- consider stopping precipitating drugs (thiazides)
- losartan has specific uricosuric action (inc excretion of uric acid) + suitable for many pts who have coexistent hypertension
- increase vit C intake may also reduce serum uric acid levels
What are adverse effects of allopurinol?
- Might initially precipitate acute attacks, but pt should continue taking
- Rashes are common → rarely SJS or TEN, if this happens then discontinue immediately
- Drowsiness, vertigo, ataxia
Since allopurinol and its metabolites are excreted by the kidney, impaired renal function may lead to retention of the drug and/or its metabolites, with consequent prolongation of plasma half-life.
The target serum uric acid level is the same as for people without renal impairment. However, when adjusting the dose, the maximum allopurinol dose increment should be 50mg.
Should a patient stop allopurinol if they are taking it and get an acute attack?
Patients already prescribed allopurinol should continue to take it at the same dose during acute episodes. This is of course in contrast to the advice that patients should not be started on allopurinol until an acute attack has settled.
What is pseudogout?
- AKA calcium pyrophosphate deposition (CPPD)
- a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium
- acute pseudogout → acute monoarthropathy usually of larger joints in elderly
- chronic pseudogout → inflammatory RA-like (symmetrical) polyarthritis + synovitis
What are risk factors for pseudo-gout?
- old age
- hyperparathyroidism
- hypothyroidism
- haemochromatosis
- acromegaly
- low magnesium, low phosphate
- Wilson’s disease
What are the key investigation findings of pseudogout?
- knee, wrist + shoulders most commonly affected
- joint aspiration → weakly-Positively birefringent rhomboid shaped crystals in Pseudogout
- X-Ray → chondrocalcinosis
