Gout

Gout Definition A very painful acute inflammatory response to monosodium urate crystals within joints Uric acid is the end product of purine metabolism in humans Epidemiology More 1% of adult men in western countries Four times more common in men than women In women more common at post-menopause Because estrogen has a uricosuric effect Most commonly affects the great toe MTP Key Info Coffee is a protective factor Most attacks only affect a single joint Gout and septic arthritis may can co-exist Risk Factors Hyperuricemia Increased uric acid production -10% Obesity Myeloproliferative disease Alcohol Psoriasis Hemolysis Rhabdomyolysis. Glycogen storage diseases Inborn errors of metabolism Red meat Fructose rich fruits E.g. apples and oranges Decreased uric acid excretion – 90% Renal impairment Starvation Polycystic kidney disease Acidosis Ketoacidosis or lactic acidosis Hypothyroidism Diabetes insipidus Sarcoidosis Lead poisoning Drugs e.g.: Aspirin Diuretics Levodopa Stages Asymptomatic hyperuricemia For most not associated with development of gout Does not need treatment Periodic attacks of acute gout with asymptomatic interludes Frequency, duration and severity increases over time Systematic illness, fever and intense pain Escalates over 6 to 12 hours Chronic gout with the development of tophaceous deposits and chronic arthropathy Clinical Features Sudden and severe attacks of joint pain Erythema Podagra Usually begins at big toe Can affect other joints Ankles, knees, wrists and elbow Chronic gout features Trophi Hard and painless nodules or uric acid crystals that form under the skin Usually in fingers, ears or joints in repeated attacks Joint damage Can lead to permanent joint damage and ROM Triggers of a Gout Attack Direct joint trauma Dehydration Acidosis Alcohol Chemotherapy Rapid weight loss Intercurrent illness Surgery Gout Attacks (Acute Gout) Usually involve only one joint -> MTP Oligoarticular and polyarticular can occur Attacks usually occur in the early in the morning Awakens patients from sleep Rapid development of severe pain and tenderness over 6 to 24 hours Distal and cooler joints at Midfoot, ankle, finger joints, wrists and knees Investigations Serum uric acid Usually raised If not -> recheck after a few weeks after an attack First line Serum urea, creatinine and eGFR Should be monitored for signs of renal impairment Jarhtocentesis -> joint fluid microscopy Most specific and diagnostic Gold standard Done when uncertain of diagnosis But hard Characteristic needle shaped monosodium urate crystals Negative birefringence Appear blue when aligned with the microscope’s axis Appear yellow when aligned perpendicular Differentiate gout from pseudogout Management of Acute Gout Spontaneously get better Foal is to relief pain and reduce duration of acute inflammation NSAIDs Effective for pain when used in full doses E.g. indomethacin 50 mg three times a day Corticosteroids Oral, IM or intra-articular E.g. prednisolone IM or intra-articular -> when wish to avoid oral Colchicine Only when NSAIDs and corticosteroids are contradicted Side effects: Nausea Vomit Diarrhoea Bone marrow suppression Neuromyopathy Rhabdomyolysis Management of Chronic Gout Patients with recurring attacks Goal: Reduce frequency and severity of attacks over the next 12 to 18 months so that they eventually disappear Urate lowering meds Need to be used long term Should not be initiated, ceased or adjusted during an acute attack Life-long therapies should be commenced when gout is severe: Recurrent flares esp. polyarticular Deforming and destructive tophaceous deposits Presence for renal calculi Allopurinol First line Blocks the conversion of hypoxanthine to uric acid Side effects: Common: itch, rash and GI issues Severe hypersensitivity: toxic epidermal necrolysis, exfoliative dermatitis, fever, eosinophilia, liver and renal dysfunction, vasculitis and bone marrow suppression Probenecid Slow titration Promotes urinary excretion of uric acid Contradicted in patients with co-existing renal stones Febuxostat Non-purine selective inhibitor of xanthine oxidase -> pxanthine forming uric acid -> decreases uric acid levels Uncertain cardiovascular risk Use with caution in patients with severe cardiovascular risk factors Complications Nephrolithiasis Trophi Chronic joint damage Most common Involves chronic pain, stiffness and disability Bursitis Chronic kidney disease and failure Higher risk of hypertension -> cardiovascular disease Metabolic syndrome Sleep apnoea Prognosis Excellent with early diagnosis and consistent management