Gout presentation

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Based on Malaysia MOH CPG Guideline

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Gout presentation

  1. 1. DR CHIA KOK KINGMedical & Health OfficerPKD Langkawi, Kedah
  2. 2. Gout A metabolic disease characterized byrecurrent attack of acute inflammatoryarthritis caused by elevated levels of uricacid in the blood (hyperuricemia). Most common rheumatic disease ofadulthood The uric acid crystallizes and deposits injoints, tendons, and surrounding tissues. Hyperuricemia :overproduction/underexcretion/bothHyperuricemia ≠ Gout
  3. 3. (NHS Fife, Gout ManagementGuidelines, 2010)
  4. 4. Asymptomatic hyperuricemia Serum [urate] abnormally high without SSx Male >420μmol/L (7mg/dL) Female >360μmol/L (6mg/dL) Not life threatening and readily treatable Routine prophylactic treatment is NOT required A/W : gout, urolithiasis, nephropathy, metabolic syndrome(HPT, DM/IFG/IGT, hyperTGemia, obesity, CKD) Serum [urate] >540μmol/L (9mg/dL) were a/w greater incidence for gout Increased daily urinary urate excretion is a/w higher risk of urate and Caoxalate stone formation (when >0.65mmol/L or 11mg/dL) Renal involvement when serum urate level is more than 2x the normallimit (0.77mmol/L or 13mg/dL in male; 0.60mmol/L or 10mg/dL) infemale)
  5. 5. Gouty arthritis1. Acute gout Acute, self limiting, monoarticular Painful, red, hot, swollen Usually resolves within 2 weeks if untreated May occur even if serum urate is normal LL > UL Commonly affected jointsI. 1st metatarsophalangeal joint (podagra)II. Forefoot/instepIII. Ankle jointIV. Knee jointV. Wrist jointVI. Elbow jointVII. Finger joints Extra-articular : olecranon bursa,Achilles tendon O/E : erythematous, warm, swelling over involved joint withextreme tenderness +/- fever  skin desquamation Duration : 2 – 3 weeks, with gradual complete resolution ofinflammatory signs
  6. 6. 2. Intercritical gout Asymptomatic period between attacks3. Chronic gout Polyarticular arthritis + tophi formation Articular tophaceous gout may results in destructivearthropathy and secondary OA Tophaceous disease more like to occur in patients with: Polyarticular presentation Serum urate level >540 μmol/L (>9mg/dL) Disease onset at younger age (≤40 years) Sites of tophi Digits of hands and feet (most common) Pinna of ear (classic, less common) Bursa around elbows and knees Achilles tendon
  7. 7. Urate/gouty nephropathy Acute urate nephropathy Urate crystals  renal tubules  obstructive ARF DeH2O, low urine pH are precipitating factors Chronic urate nephropathy Urate crystals  interstitium and renal medulla inflammation + surrounding fibrosis  irreversible CRF Renal impairment can occur in ~40% in chronic gout Urate nephrolithiasis Stones  flank pain/ureteric colic/hematuria Urate (radiolucent) / mixt. Calcium oxalate and/or calciumphosphate (radio-opaque) Contributing factors : hyperuricosuria, low urineoutput, acidic urine Urinary alkalinization (pot. Citrate or NaHCO3)  dissolutionof existing stones and prevention of recurrence
  8. 8. Diagnostic criteria Two of the following criteria are required forclinical diagnosis :1. Clear h/o at least 2 attacks of painful jointswelling with complete resolution within 2weeks2. Clear history or observation of podagra3. Presence of tophus4. Rapid response to colchicine within 48 hours oftreatment initiation Definitive diagnosis : presence ofmonosodium urate crystals seen in synovialfluid/tissues
  9. 9. Investigations Specific investigations for confirmation Serum uric acid Joint aspiration and crystal identification Not widely available To detect medical conditions a/w gout or hyperuricemia FBC Serum creatinine/urea Serum blood glucose Fasting lipid profile UFEME 24h urinary urate excretion : Useful if renal calculus proven to be urate stone Indicated if on uricosuric agent Assess risk of stone Help to indicate whether overproduction or underexcretion of urate Range : 2-4 mmol/24h or 0.34-0.67g/24h To detect complications Renal imaging Skeletal x-rays
  10. 10.  Skeletal x-rays Acute gouty arthritis : normal; soft tissue swelling Chronic tophaceous gout : tophi, erosive bonelesions (punched out lesions), joint space ispreserved until late stage, pathognomonic in footand big toe
  11. 11.  Renal imaging Plain abd XR detects only 10% of all urate stones IVU = investigation of choice for urate stones US KUB : investigations of choise fornephrocalcinosis, significant renal stones (>3mm)whether radio-opaque or radiolucent, obstructivenephropathy Plain CTU : most sensitive to detect any stone
  12. 12. Management Lifestyle modification and dietary advice Management of comorbidities Nonessential prescriptions that induce hyperuricaemia Main aim :-To achive ideal BW- Prevent acute gouty attacks- Reduce serum urate level Strict purine-free diet reduced only 15 – 20% of serumurate, thus is considered an adjunct therapy tomedication.
  13. 13. Treatment Contributing factors eg. thiazide/loop diuretics; lowdose aspirin may be discontinued or substituted, ifappropriate Pharmacotherapy of asymptomatic hyperuricemiais NOT necessary, except :- Persistent severe hyperuricemia- > 770μmol/L (13mg/dL) in male- > 600μmol/L (10mg/dL) in female Persistent elevated urinary excretion of urate- > 0.65mmol/L/day (11mg/day), a/w 50% increased risk ofurate calculi Tumor lysis syndrome- chemotherapy/radiotherapy  extensive tumor cytolysis=> require pre-hydration and allopurinol to prevent acuteurate nephropathy
  14. 14. Treatment : Acute gouty arthritis Initiation within 24 hours of onset If on Allopurinol, continue without interruption NSAIDs eg. Diclofenac, indomethacin, mefenemic acid etc Caution in h/o PUD, HPT, renal impairment, IHD, liver impairment COX-2 inhibitors (celecoxib, etoricoxib, parecoxib) = alternative for aboverisk factors Studies have shown that etoxicoxib (Arcoxia) has equal efficacy toindomethacin Colchicine Inhibiting mitosis and neutrophils motility and activity, leading to anet anti-inflammatory effect. Alternative drug if CI to NSAIDs, but is poorly tolerated by elderly Therapeutic index is narrow Slower onset of action Evidence base for prophylaxis is stronger than for NSAIDs (NHS Fife, GoutManagement Guidelines, 2010) SE (eg. N&V, abd. pain, profuse diarrhea) limit its usefulness Dosage : 0.5mg – 0.6mg BD-QID
  15. 15.  Steroids Can be considered in elderly people and patients withrenal/liver impairment, IHD, PUD, hypersensitivity toNSAIDs IM steroids eg.Triamcinolone (40-80mg.day) ormethylprednisolone (80mg/day) can be given stat Short course of oral prednisolone up to 0.5mg/kg/daycan be given and tapered off over 4 -10 days SE of steroids are rare(NHS Fife, Gout ManagementGuidelines, 2010)
  16. 16. Treatment : chronic gouty arthritisManagement of Gout, CPG 2008, MOH Malaysia
  17. 17. Urate lowering therapy(hypouricaemic therapy) Allopurinol should not be started until acute attackhas resolved May prolong attack or lead to rebound flares ifstarted during attack Should be started 2 weeks after attack is well-controlled Indications for ULT :1. Frequent and disabling attacks of gouty arthritis (3 ormore attacks/year)2. Clinical or radiographic signs of erosive gouty arthritis3. The presence of tophaceous deposits4. Urate nephropathy5. Urate nephrolithiasis6. Impending cytotoxic chemo-/radiotherapy for lymphomaor leukemia
  18. 18.  D/W with patients regarding important pointsat initiation of ULT1. NSAIDs/colchicine do not lower serum urate2. Hypouricemic drugs have no analgesic or anti-inflammatory effect3. ULT agent should not be stopped during anattack after initiation4. Possibility of more frequent attacks of acutegouty arthritis at the initiation oftherapy, especially in the first 3 months.Prophylactic NSAIDs/colchicine can be used toreduce frequency of attack5. Is a life-long treatment6. Lifestyle modification is an important adjuncttherapy
  19. 19. Management of Gout, CPG 2008, MOH Malaysia
  20. 20. Xanthine oxidase inhibitorALLOPURINOL More superior than probenecid Primarily excreted by kidneys, thus need renaladjustment Aim : reduce to <360μmol/L and maintain withminimal dose of allopurinol During initiation of allopurinoltherapy, colchicine (0.5mg BD) can be used asprophylaxis to reduce frequency of attacks. Canbe continued until patient is attack free for 6months or target serum urate level is achievedfor 1 month. For patient who can’t tolerate colchicine, lowdose NSAIDs can be used
  21. 21.  Normal renal function : Start at 100 – 150mg OD, increasing by 100 – 150mg stepsevery 2 - 5 weeks till 300mg OD, max 900mg/day (severedisease) With prophylactic colchicine 0.5mg BD for up to 12 months(NHS Fife, Gout ManagementGuidelines, 2010) Starting dose should be not >100mg/day and less inmoderate to severe CKD, with gradual upward titration(ACR,Guidelines for Management of Gout, 2012) Indications for starting allopurinol must be clear, aslife threatening complications can occur Rash Bone marrow suppression Aplastic anemia Agranulocytosis Granulomatous hepatitis and jaundice Hypersensitivity syndrome(fever, rashes, hepatitis, eosinophilia, renal impairment)
  22. 22. Uricosuric agent PROBENECID An alternative to allopurinol in patients with NORMAL RENALFUNCTION RP before commencement of probenecid Dosage : 0.5 – 1g in divided doses, may be increased to 1.5 – 2g SE : GI disturbance Hypersensitive rash CI :- uric acid overproduction and overexcretion (24 hrs urinary urateexcretion morethan 800mg/day)- urate nephropathy- urate nephrolithiasis Losartan has modest uricosuric effect  Fenofibrate too Risk of crystal precipitation
  23. 23. (NHS Fife, Gout ManagementGuidelines, 2010)
  24. 24. Treatment of urate nephropathy Increase urine output 3L of H2O/day with urine output >2.5L if not ESRF Increase urine pH Prevent urate stone formation and promote dissolution ofstone Target urine pH : 6.5 – 7 Potassium citrate 40 – 50mmol/day (max 100mmol/day) Sodium salt : Ural sachet (with analgesic properties)Dosage : 1 – 2 sachets QIDCI in renal impairment/hypernatraemia Decrease urate excretion Dietary purine intake restriction Treat with allopurinol
  25. 25. Treatment of urate nephrolithiasis Intrarenal stones <5mm can be observed unlesscausing pain Intrarenal stone 5 – 15mm or complex staghorncalculi  refer to urologist for ESWL or PCNL Ureteric stones : conservative management If uncomplicated (min obstruction/no sepsis), and size<5mm, at lower ureter  may pass spontaneously If fail to pass after 2 weeks  refer for removal Pure urate stones can be chemolysed by pot. Cit. orUral (oral/direct irrigation) Long term chemoprophylaxis using pot. Cit. hasshown to be highly effective
  26. 26. Surgical intervention Last resort for gouty arthritis Removal of tophi Joint fusion Joint replacement Ulceration of tophi : debridement, dressing withsodium bicarbonate solution Indications for chronic tophaceous gout : Advanced tophi deposition resulting in major jointdestruction Loss of involved joint movements a/w severe pain Tophi collection causing pressure symptoms, eg carpaltunnel syndrome of wrist Tophaceous ulcer Cosmetic eg ear lobe tophi
  27. 27. When to reduce ULT????? If serum urate <360μmol/L , and have been nogouty attacks for 1 year  can reduceT.allopurinol by 100mg. Check serum urate 6 monthly, if still<360μmol/L  can further reduce Patients that have tophi are most likely torequire lifelong ULT
  28. 28. Referral to specialist Unclear etiology Refractory SSx (fails to respond within 14days with treatment) Difficulty in achieving target serum uratelevel/recurrent attacks despite onT.allopurinol 900mg OD Uncontrolled acute gout attacks when serumurate <360μmol/L Renal impairment Adverse effects of ULT/Intolerance
  29. 29.  (NHS Fife, Gout ManagementGuidelines, 2010)
  30. 30. References Management of Gout, CPG 2008, MOHMalaysia 2012 American College ofRheumatology, Guidelines for Managementof Gout), part 1, part 2 NHS Fife, Gout ManagementGuidelines, 2010

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