Hot Swollen Joint Flashcards
Differentials of painful swollen joint
-Septic arthritis
-Inflammatory arthritis
-Crystal arthritis
-Haemarthrosis
-Trauma
-Bursitis/ cellulitis
Describe crystal arthritis
-Variety of crystals can deposit within joints; uric acid, calcium pyrophosphate, basic calcium phosphate
-Requires sufficient substrate, with joint damage predisposing to crystal formation by reducing inhibitors of crystallisation (e.g. osteoarthritis joint damage)
-Increasingly common
-Very painful
Characteristic presentation of crystal arthritis
-Typically monoarthritis
-1st MTP involved in >50% of first presentations of gout, knee most commonly involved in CPDD
-Severe pain (max intensity 12 hours) and erythema characteristic, acute swelling
What is gout?
-An inflammatory arthritis caused by the immune reaction to urate crystals in the joint
-Typically presents within 24 hours with worst pain ever experienced
-Untreated can progress to joint destruction with tophaceous deposits
Time course of gout
-Asymptomatic hyperuricaemia (>0.45) (0-5yrs)
-Recurrent acute gout (5-10 years)= only a minority of hyperuricaemia individuals develop gout (convalescent hyperuricaemia key predictor)
-Advanced gout (10+)
Prevalence of gout
-Most common inflammatory arthritis
-Prevalence 2.5% in UK
-3-4 times more common in men than women
-Increasing globally along with ageing and obesity
-Decreased uric acid excretion: diuretics, CKD, lead toxicity
-Increased production: myeloproliferative disorder, cytotoxic drugs, severe psoriasis
Gout score system
-Male sex= 2.0
-Previous reported arthritis attack= 2.0
-Onset within 1 day= 0.5
-Joint redness= 1.0
-MTP 1 involvement= 2.5
-Hypertension or >1 cardiovascular disease= 1.5
-Serum uric acid >5.88mg/dl (0.35mmol/l)= 3.5
Score >8 gives 80% likelihood of gout
Investigations of gout
-Joint aspiration to exclude septic arthritis
=Strict aseptic technique - synovial fluid sent to microbiology for gram stain & culture as first priority
=If sufficient aspirate inoculate blood culture bottles with synovial fluid. Extra fluid sent for pathology
=Neither warfarin nor skin erythema is absolute contra-indication. Special care with prosthetic joints – call surgeon
=Blood cultures x 2 (essential)
-Joint aspirate (usually requiring large joints)= synovial fluid or tophi= needle shaped negatively birefringent monosodium urate crystals under polarised light
-Serum urate unreliable in acute gout as can be normal, if found elevated makes gout more probable but cannot rule out septic arthritis (needs 48hrs negative cultures), urate also normal in attack due to effect of inflammation on urate excretion
-X-ray= joint effusion, well-defined punched out erosions juxta-articular, no periarticular osteopenia, soft tissue tophi
Acute management of gout
-First line therapy is full strength NSAID (any) taken promptly after onset of attack (1-2 days after resolution)
-Low dose colchicine has shown equal efficacy to high dose regimes with lessened toxicity1 eg 500mcg 2-4 times daily
=Bowel upset/ caution in renal impairment
-Cortico-steroid have equal efficacy to NSAIDs eg prednisolone 30mg od for 5 days, if NSAID contra-indicated
-Also consider IM or IA steroid
Long term management of gout
-Reduce serum uric acid by possibly discontinuing medications causing hyperuricaemia
-Lifestyle modification (weight loss and alcohol/surgery drink reduction)
-All patients should be offered urate lowering therapy (allopurinol- 100mg and increase in 100mg increments until SUA target reached max 900mg/ or febuxostat)
Why is gout a curable disease that is often not cured?
-Patient barriers:
=Non-adherence to ULT
=Lack of knowledge & understanding exacerbated by paradoxical flares (precipitated by initiation of ULT- colchicine prophylaxis 500mg bd for 6 months)
=Male reluctance to seek medical attention
=Distorted negative stereotypical view of gout
-Provider barriers:
=Guidelines not used in General Practice
=Patient education and information not given
=Managed as acute rather than chronic disease
=Lack of knowledge & understanding
=Lack of training and education
=Lack of incentives
SUA targets in gout
-Achieving urate below saturation level should prevent new
formation of crystals (serum target <0.36 mmol/l)
=but still allows infrequent attacks
=persistence of urate crystals may be seen in synovial aspirates
=resolution of tophi is speeded in direct proportion to the success of urate lowering
-In newly diagnosed patients (BSR), or patients with tophi (ACR) should aim for serum urate target < 0.3mmol/l
=Wait more than 2 weeks (4-6) before measuring serum urate after lowering therapy
=Median dose of 400mg allopurinol required to achieve
What is pseudogout?
-Calcium pyrophosphate dihydrate crystal deposition disease
-Cartilage calcification of x-ray, rhomboidal positively birefringent crystals on aspirate
Causes of pseudogout
-Usually idiopathic on background OA
-Rare families described with Autosomal dominant
inheritance (linked with pyrophosphate transporter ANKH)
-Acquired – Inhibitory ions (inhibit pyrophosphate
metabolism)
=Ca - Primary hyperparathyroidism
=Fe- Haemochromatosis
=Cu- Wilson’s disease
=Acromegaly, low magnesium and phosphate
-Acquired – Deficiency of Mg (ALP co factor)
=eg Chronic diarrhoea
Hot swollen joint in immunocompromised (anti-TNF)
-Opportunistic infections with Mycobacteria, Histoplasmosa, listeria and salmonella species
-Increased frequency of TB, listeria and salmonella
confirmed in BSRBR
-Opportunistic infections reported most commonly in anti TNF treated patients in N American cohorts
were V Zoster and Pneumocystis jiroveci
