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2014 GSS Updates on Gout
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Basic information about Gout and Gouty arthritis, Hyperuricemia
For UnderGraduates and Orthopaedic Surgeons

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  1. 1. Gout Dr. Apoorv Jain D’Ortho, DNB Ortho +91-9845669975
  2. 2. Gouty Arthritis • Chronic heterogeneous disorder of urate metabolism • Results in deposition of monosodium urate crystals in the joints and soft tissues, with accompanying inflammation and degenerative consequences • Most common form of inflammatory joint disease in men aged ≥40 years
  3. 3. History • 2640 BC: Podagra first identified by the Egyptians. • 5th Century BC: Hippocrates referred to gout as “unwalkable disease” and noted links between gout & lifestyle, demographics & other variables
  4. 4. • The word ‘gout’ is derived from the Latin word ‘gutta’. • Earlier it was believed that an acute attack of the disease was the result of poison dropping into a joint • Disease of the ‘KINGS’ (Rich foods have a higher concentration of protein. This could cause major problems for a person afflicted with gout)
  5. 5. The King of Pain • Benjamin Franklin • Thomas Jefferson • Sir Isaac Newton • Charles Darwin • King Henry VIII and other famous leaders all suffered from gout
  6. 6. Incidence • Persons in USA Affected by Common Rheumatologic Disorders (As per ACR):  Frequent Low Back Pain 40.2 million in 2005, projected to increase to 48.6 million in 2025  Osteoarthritis 20.7 million in 2005, projected to increase to 28.1 million in 2025  Gout 2.6 million in 2005, projected to increase to 3.6 million in 2025  Rheumatoid Arthritis 2.1 million in 2005, projected to increase to 2.8 million in 2025
  7. 7. Predisposing Factors • Purine rich foods – meat, kidney, liver, seafood, anchovies, oatmeal, certain vegetables (peas, beans, lentils, mushrooms, cauliflower, spinach), sweetbreads • Caffeine • Drugs – Loop diuretics, NSAIDs, corticosteroids, Niacin, Sinemet, Cyclosporine, Salicylates, Ethambutol, Pyrazinamide • Trauma • Infection • Other disease – DM, HTN, vascular dx, renal dx, thyroid dx, sarcoidosis, etc.
  8. 8. Hallmarks of Gout • Group of conditions which may be characterized by an elevation of serum uric acid (usually) • Recurrent attacks (flares) of an acute inflammatory arthritis with monosodium urate crystals demonstrated in synovial fluid leukocytes • Bone and joint destruction in some cases
  9. 9. • Aggregates of uric acid crystals (tophi) in and around joints, soft tissues, and various organs • Tophus in bone leading to erosions in some cases • Kidney disease and stones
  10. 10. Hyperuricemia leads to deposit of urates in the joint fluid, triggering an inflammatory cascade
  11. 11. Stages This disorder can be progressive through four stages if undertreated Asymptomatic hyperuricemia Acute gout Intercritical gout Chronic tophaceous gout
  12. 12. Clinical Features
  13. 13. Acute Gout: • Acute gout is a painful condition that typically affects only one or a few joints. • The big toe, knee, or ankle joints are most often affected. • Throbbing, crushing, or excruciating pain • Joint appears warm and red. Fever may be there.
  14. 14. • The attack may go away in a few days, but may return from time to time. • Additional attacks often last longer. • After a first gouty attack, half of the people will have no symptoms. Half of patients have another attack.
  15. 15. Chronic Gout • Signs and symptoms include: • Joint damage • Loss of motion in the joints • Joint pain and other symptoms most of the time, throughout the day • Tophi below the skin around joints or in other places (Tophi usually develop only after a patient has had the disease for many years)
  16. 16. Advanced Chronic Tophaceous Gout • Tophi can be seen clinically, with obvious deformity demonstrated in hands and foot • Tophi may be associated with bony destruction as seen on the x-ray
  17. 17. • Is characterised by massive deposits of monosodium urate crystals (Tophi) in articular cartilage, subchrondral bone, synovial membrane, capsule, tendon sheaths and peri articular tissues. • Tophi formation can also occur over eyelids, nasal cartilage, cornea, tongue, vocal cords and penis
  18. 18. • The tophaceous nodules consists of multicentric deposition of urate crystals and intra cellular matrix and foreign body granulomatous reaction. • As they enlarge in size, calcify, they can cause pressure symptoms. • The tophi are firm yellow in colour and occasionally discharge a chalky material.
  19. 19. Diagnosis
  20. 20. 1977 ACR Criteria for Acute gout The presence of characteristic urate crystals in the joint fluid, or a tophus proved to contain urate crystals by chemical means or polarized light microscopy, or the presence of 6 of the following 12 clinical, laboratory, and radiographic phenomena: 1. More than one attack of acute arthritis 2. Maximum inflammation developed within 1 day 3. Monoarthritis attack 4. Redness observed over joints
  21. 21. 5. First metatarsophalangeal joint painful or swollen 6. Unilateral first metatarsophalangeal joint attack 7. Unilateral tarsal joint attack 8. Tophus (proven or suspected) 9. Hyperuricemia 10. Asymmetric swelling within a joint on x ray/exam 11. Subcortical cysts without erosions on x ray 12. Joint fluid culture negative for organisms during attack
  22. 22. Investigations • Plain radiographs (may be normal) • Serum Uric acid • Synovial fluid analyis (shows uric acid crystals) • BUN (blood urea nitrogen), Serum Creatinine • Synovial biopsy • Uric acid – urine
  23. 23. SYNOVIAL FLUID ANALYSIS (Polarized Light Microscopy) • The Gold standard • Crystals intracellular during attacks • Needle & rod shapes • Strong negative birefringence
  25. 25. Differential Diagnosis • Pseudogout: Chondrocalcinosis, CPPD • Psoriatic Arthritis • Osteoarthritis • Rheumatoid arthritis • Septic arthritis • Cellulitis
  26. 26. Gout vs. CPPD • Similar Acute attacks • Different crystals under Microscope: Rhomboid, irregular in CPPD
  27. 27. Gout vs RA • Both have polyarticular, symmetric arthritis • Tophi can be mistaken for RA nodules
  28. 28. To be continued.. Treatment Gout
  29. 29. Drugs Used In Treatment • NSAIDs • Colchicine • Uricosuric agents • Allopurinol/ Febuxstat
  30. 30. NSAIDS: • Inhibits pain & inflammation. • Inhibits urate crystal phagocytosis by decreasing the migration of granulocytes into the inflammatory area. • Indomethacin, Naproxen, Ketorolac.
  31. 31. COLCHICINE: • Produces its anti-inflammatory effects by binding to the intracellular protein tubulin, preventing its polymerization leading to the inhibition of leukocyte migration into affected area. • Inhibits the synthesis & release of leukotrienes.
  32. 32. URICOSURIC AGENTS: • Probenecid & Sulfinpyrazone • They are weak organic acids . • Sulfinpyrazone is a metabolite of phenylbutazone. • Increase the excretion of Uric acid.
  33. 33. Allopurinol/ Febuxstat: • Inhibits synthesis of uric acid by inhibiting xanthine oxidase enzyme
  34. 34. Uric acid is produced by Xanthine and Hypoxanthine by Xanthine Oxidase Inhibitor. Uric Acid is more toxic than either xanthine or hypoxanthine.
  35. 35. TREATMENT GOALS 1. Rapidly end acute flares 2. Protect against future flares 3. Reduce chance of crystal induced inflammation 4. Prevent disease progression 5. Lower serum urate to deplete total body urate pool 6. Correct metabolic cause
  36. 36. ENDING ACUTE FLARES • Control inflammation & pain to resolve the flare • Not a cure • Crystals remain in joints • Don’t try to lower serum urate during a flare
  37. 37. Acute Flares Treatment • Interaction with warfarin • Contraindicated in: • Renal disease • PUD • GI bleeders NSAIDS •Not as effective “late” in flare •Contraindicated in dialysis patients •Cautious use in : •Renal or liver dysfunction •Active infection •Age > 70 Colchicine • Worse glycemic control • May need to use mod-high doses Corticosteroids
  38. 38. Acute Gout - Rx NSAIDs (unless CRI, CHF, PUD, etc.) Corticosteroids (Intra-articular if one joint, systemic if multiple joints) Colchicine (adjust dose in patients w/ renal insufficiency) - Indomethacin 50mg tid - Naproxen 825mg once, then 275 q8hr - Sulindac 200mg bid - Most beneficial in first 12-36 hours of an attack - 1mg initially, then 0.5mg qhr until either symptoms relieved or GI side fx (N/V/diarrhea) or 7mg total given - Renal dosing: - If Cr clearance < 50, dec. dose 50% - If Cr clearance < 10, contraindicated. - 20-30mg/day if systemic used
  39. 39. Protection Against Future Flares • Colchicine : 0.5-1.0 mg/day • Low-dose NSAIDS • Both decrease frequency & severity of flares • Prevent flares with start of urate- lowering drugs • Best with 6 months of concomitant treatment
  40. 40. Intercritical Gout - Rx Probenecid if: - Recurrent attacks and 24hr urine uric acid < 800mg/dL Allopurinol therapy if: - Recurrent attacks despite diet chg/etc. - Hx of nephrolithiasis - Serum creatinine > 2.0 - Serum uric acid > 11.0 - 24 hr urine uric acid > 800mg/dL - Tophi present Education, Lifestyle/Diet modification, Pharmacotherapy modification Allopurinol toxicity? Colchicine
  41. 41. Prevent Disease Progression • Lower urate to < 6 mg/dl : • Depletes Total body urate pool Deposited crystals • Treatment is lifelong & continuous • Drug choices : Uricosuric agents Xanthine oxidase inhibitor
  42. 42. Asymptomatic Hyperuricemia • Indications for Rx include:  24hr Urinary Uric Acid Excretion > 1100mg  Serum uric acid: Men > 13mg/dL, Women > 10mg/dL  Nephrolithiasis  Any hx of symptoms of gout, especially w/ worsening renal function  Presence of gouty tophi in bone or soft tissues  Radiographic signs of gouty arthritis  Impending chemotherapy or radiotherapy for leukemia or lymphoma
  43. 43. Which Drug to use? • Base choice on above considerations & whether patient is an overproducer or underexcretor. • Need to get a 24-hr. urine for urate excretion: < 700 --- underexcretor (uricosuric) > 700 --- overproducer (allopurinol) • 90% of the patients are underexcretors.
  44. 44. PREVENTION  Avoid purine rich foods  Reducing alcohol consumption  Avoid Diuretic Drugs. Maintain the concentration of Uric Acid level within the normal range.  Drinking Plenty of Water.  Balance your weight with proper diet and exercise
  45. 45.  Foods known to decrease the occurrence of gout include dairy, foods high in potassium, black cherry juice, blueberries and lemon juice.  Immediately treating gout will not allow it worse.
  46. 46. Newer Drugs URICASE ENZYMES: • Catabolize urate to allantoin: More soluble, excretable form • Currently approved for hyperuricemia in tumor lysis syndrome • Some concerns: fatal immunogenicity & unknown long-term effects
  47. 47. Thank You


  • Uric acid in urine Is low due to hyperurecmia as kidneys are unable to excrete the uric acid
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