Gout Flashcards
What is the difference between gout and pseudogout seen on polarised light microscopy?
- Gout: negatively birefringent, needle-shaped crystals of sodium urate
- Pseudogout: weakly positively birefringent, rhomboid-shaped crystals of calcium pyrophosphate
N for gout
- Na Urate
- Negative Birefringent
- Needle shaped
P for pseudogout
- Pyrophosphate
- Positively Birefringent
How do the presentations of gout and pseudogout differs in terms of age group?
Gout
- Younger
- Younger men >30yo
Pseudogout
- Older
- Elderly women
What are the risk factors for gout?
- OA joints (prone to gout attacks as crystal ppt better on uneven surface)
- Metabolic syndrome (insulin R enhances uric acid reabsorption)
- Diuretic use (thiazide, loop), low dose aspirin (blocks uric acid secretion). This is why Furosemide (Lasix; a loop diuretic) can lead to gout!
- FHx gout
- Diet: purine-rich foods (red meat, certain fish/shellfish), alcohol, high saturated fats, fructose-containing drinks. Ask for recent binge drinking; red meat / seafood buffet
- Problems with excretion: CKD (but rarely ppt gout)
- Tumor Lysis Syndrome: lympho / myeloproliferative disorders; Solid Ca
- Inborne Errors of Metabolism: Lesch-Nyhan syndrome
How does gout present acutelyy?
The ACUTE ONSET + Pain peaks within 24 hrs + Relapsing & Remitting course helps zone in on Gout!
Initially monoarticular, but w recurrence may become polyarticular (<20%)
- Severe pain of the 1st MTPJ waking the patient up in the middle of sleep
- Severe redness, erythema, swelling, pain, unable to weight bear
- Sudden onset, **peaks in 12-24hrs, can last days-weeks (typically 1/52 if untreated)
Dz course
- ** Relapsing and Remitting course
- Resolution is complete, a/w desquamation of overlying skin
- Followed by asympt intercritical phase; 2nd flare likely within 2 years
With associated RF
- Alcohol ingestion (alc metabs compete for same excretion sites in kidney)
- Feast of red meats, seafood
- Drugs (thiazides, furosemide, aspirin, pyrazinamide)
- Dehydration, fasting
- Surgery, trauma
How does chronic interval gout present?
- Acute attacks superimposed on low-grade inflammation and potential joint damage
- May have polyarticular flares, peri-articular involvement (tendons, bursae), bony erosions and deformities
- If untreated over years, Inter-critical period may shorten as flares become more freq and prolonged
How does chronic tophaceous gout present?
- Indicates severe, recurrent and chronic gout (usually 10-15 years), due to over pdtn (and not just undersecretion)
- Urate crystals accumulate forming tophi commonly in olecranon bursa, helix of ear, fingers, tendon achilles
- tophi are typically painless, non-tender, initially soft but hardens as they mature
- large tophi may ulcerate through skin and discharge its chalky white material
- A/w renal impairment, LT diuretic use, acute/chronic urate nephropathy, urate urolithiasis
What are the complications of gouty tophi?
- Chronic pain, stiffness and deformity: 2’ to chronic inflammation and destruction (eg bony erosions)
- Cosmesis: try not to excise as overlying skin is typically stretched out and unhealthy -> high risk of wound breakdown and infection after excision. Manage medically.
- Infection: requires emergency excision, ask pt to look out for pain
What is the relevant history to take in a patient with gout?
Ask regarding the gout
1) HOPC: severity of pain, associated symptoms, ROM, WB, peaking in 12-24 hours
2) Risk factors: metabolic syndrome, alcohol, buffet, thiazide/ furosemide
3) Non-modifiable RF: Haematological malignancies
4) Cx: Renal calculi, haematuria
Ask regarding DDx – i.e. septic arthritis
1) Fever
2) Direct inoculation: trauma, instrumentation, needle
3) Recent illness (haematological spread)
4) Bone / soft tissue infection
5) immunocompromised state
6) Pain peaking in ~3 days
7) Consider also asking for DGI: haematuria, discharge, dysuria, freq, urgency, migrating arthritis, pustular painless rash, STI history
What are the investigations to be performed in a patient with gout? -
Joint aspiration: GOLD STANDARD
- Cell count w differential count: to assess inflammatory / septic arthritis
- Gram stain, c/s & sensitivity: TRO septic arthritis
- Polarised microscopy: spindle-shaped strongly negatively birefringent crystals in PMNs, crystals must be intracellular (ie within PMN cells) to be indicative of an acute attack
Labs
- FBC for signs of inflam: ↑ WCC
- Blood c/s
- Renal panel for renal impairment (may be a cause (hyperuricemia) or consequence (chronic urate nephropathy))
- +/- Urinalysis for haematuria, uric acid crystals: if +ve, US kidneys to look for renal stones (US needed to see kidney parenchymal and radiolucent urate stones)
- Serum uric acid for hyperuricaemia, ≥2wks after resolution: ↑ uric acid (do not check during acute attack: reading will be falsely low as the acid is ppted in the joint)
- +/- Metabolic panel to screen for CVRF: HbA1c, fasting glucose, fasting lipids
- Inflammatory markers not necessary
Imaging- XR of affected joint
- Acute gout: soft tissue swelling (increased density/opacification)
- Chronic tophaceous gout
What are the x ray features of chronic tophaceous gout?
- Tophi (deposition of urate crystals, +/- calcium precipitation)
- Peri-articular erosions, ‘punched out’ bony cysts, over-hanging cliffs, sclerotic margins (characteristic punched-out lesions)
- Intra-osseous lesions
- Preserved joint space (until late stages), no peri-articular osteopenia
What is the NIJMEGEN score (Clinical Diagnostic rule for Gout w/o Joint Aspiration in primary care setting)?
< 4 points: low probability
> 8 points: high probability
- Male sex = 2
- Previous arthritis attack = 2
- Onset within 1 day = 0.5
- Joint redness = 1
- Involvement of the 1st MTPJ (Podogra) = 2.5
- Hypertension or >1 CVS diseases = 1.5
- Serum uric acid >350umol/ L = 3.5
What is the management during an acute flare of gout?
1) High potency NSAIDs eg diclofenac TDS/ COX-2 single day dosing (more potent but more ex)
2) Colchicine only if within 24-48 (see below ↓) from start of flare: PO 500mg TDS
- Prevents migration of lymphocytes into joint space at start of flare, hence useless after 48h
3) Steroids (PO/IM/intra-art)
- Indications: NSAIDs and colchicine C/I eg renal impairment OR severe/polyarticular flare
- Note: taper off over 10-14 days to reduce risk of rebound attack
DO NOT START / STOP ALLOPURINOL DURING ACUTE FLARE OF GOUT
What are the C/Is of high potency NSAIDS in the treatment of gout?
renal impairment
What are the S/Es & C/Is of high potency NSAIDS in the treatment of colchicine?
C/I: renal impairment (metabolites accumulate -> pancytopenia, drug induced myopathy)
S/E: diarrhoea, abdominal pain
What is the chronic management of gout to prevent recurrence through lifestyle and pharmacological methods ?
Lifestyle modification and diet
- Weight loss, control CV RF
- Stop / change diuretics to less urate retaining ones
- Dietary advice
- ↓ purine-rich foods (organ meats, sardines, beef, sweet breads)
- ↓ alcohol intake (esp. beer; high in purines and fructose)
- ↓ non-diet carbonated soft drinks (high in fructose)
- ↓ total calorie and cholesterol intake
Treat concurrent disease – for HTN pts, use losartan which helps to lower uric caid
Consider urate lowering therapy (ULT)
- Most commonly, Allopurinol is given; However, there is risk of SJS / TEN -> hence only give when indicated!
- Febuxostat, a newer non purine xanthine oxidase inhibotr, may be considered an alternative to allupurinol
- Probenecid: uricosuric drug; increases uric acid renal excretion
- Benzbromaron: uricosuric drug. increases uric acid renal excretion
