Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

GOUTY ARTHRITIS-PSEUDOGOUT-TREATMENT:Dr.Sandeep Agrawal,Agrasen Hospital,Gondia Maharashtra India

4,594 views

Published on

GOUTY ARTHRITIS AND PSEUDOGOUT ( CHONDROCALCINOSIS ) : Dr.Sandeep Agrawal, Agrasen Hospital , Gondia Maharashtra INDIA
Rheumatoid Arthritis,Psoriatic arthritis,Reiters syndrome

Published in: Science

GOUTY ARTHRITIS-PSEUDOGOUT-TREATMENT:Dr.Sandeep Agrawal,Agrasen Hospital,Gondia Maharashtra India

  1. 1. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS GOUT
 Dr.Sandeep Agrawal MS,DNB (ORTHOPAEDICS)
 Agrasen Hospital
 Gondia
 Maharashtra INDIA
 drsandeep123@gmail.com
 09960122234
 
 GOUT PSEUDOGOUT Symptoms,Control,Diet & Treatment
  2. 2. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Introduction: 2 Introduction Diagnosis Purine metabolism Complications Management GOUT
  3. 3. ! Uric acid has! ! 1. Low water solubility.! 2 . Especially in low pH! ! ! ! Blood levels high…. precipitates …. deposit as sodium urate crystals on joints, kidneys and subcutaneous tissue( tophi) • Gout is a syndrome caused by the inflammatory response to tissue deposition of monosodium urate crystals (MSU). ➢ Uric acid can accumulate due to: ➢Overproduction of purine nucleotides ➢Enhanced cell turnover (purine degradation) ➢Decreased in purine salvage pathway ➢Underexcretion of uric acid
  4. 4. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 4
  5. 5. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Gout: pathophysiology 5 Food intake Cell breakdown Purines Uric acid HYPERURICAEMIA Kidney Soft tissue of the joints Other tissue Ear Overproduction Under excretion
  6. 6. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Click to edit Master title style 6 Historical Review Podagra (Greek Pous), gout (Latin Gutta), honoured in antiquity Hippocrates (460-370 B.C.): the ‘unwalkable disease’ Scheele, 1776: uric acid in urine Wollaston, 1797: ear tophus Garrod, 1848: uric acid in blood Talbot, 1967, quoted famous patients: Darwin, Harvey, Hunter, Newton and sydenham Huber, 1896: x-ray characteristics of gouty arthritis (Clin. Radiol. 1975)
  7. 7. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 7 Introduction • Hyperuricemia: at 37ºC, value of urate saturation about 7 mg/dl; 2.3 to 17.6 % of the populations • Natural Hx of gout: 4 stages a. asymptomatic hyperuricemia b. acute gouty arthritis: MSU crystal deposition; 4th to 6th decades; great toe, ankle, heel, knee, wrist, finger, and elbow in order of frequency. c. intercritical gout d.chronic tophaceous gout: aggregates of MSU crystals in and around joints
  8. 8. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Precipitating Risk Factors 8 • Lower temperature • Decreased binding to plasma protein • Trauma • Local tissue change • Decreased PH • Protracted hyperuricemia ! • Urate crystals..unique distribution … • sites rich in connective tissue…… • synovium, cartilage, tendon, skin, renal interstitium.
  9. 9. Interrelationships (HU, CRD, CVD) CELL PURINE URIC ACID XO HYPERURICEMIA SMC Proliferation Vasoconstriction RAS Activation COX2 Activation HYPERTENSION ! ENDOTHELIAL DYSFUNCTION & CARDIOVASCULAR DISEASE ! RENAL DISEASE PROGRESSION Tissue Hypoxia Cell Death Insulin Resistance
  10. 10. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Hyperuricemia 10 production excretion hyperuricemia results when production exceeds excretion
  11. 11. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Hyperuricemia 11 production excretion net uric acid loss results when excretion exceeds production
  12. 12. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 12 hyperuricemia excessive production inadequate excretion
  13. 13. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Hyperuricemia Mechanism 13 hyperuricemia overproducers underexcretors
  14. 14. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Urate-lowering drugs 14 net reduction in total body pool of uric acid block production enhance excretion
  15. 15. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Classifying hyperuricemia 15 • serum uric acid level • urine uric acid excretion (24-hour)
  16. 16. Gout: Pathophysiology Uric acid: overproduction vs. underexcretion Mechanisms of urate “production” ▪ cellular nucleoproteins/nucleotides (~ 66%) ▪ diet (~33%) Mechanisms of urate excretion ▪ kidney (~66%) ▪ gut (~33%)
  17. 17. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Renal Handling of Uric Acid 17 • Completely filtered by the glomerulus • Completely (essentially) reabsorbed in the proximal tubule • Approximately 50% is secreted back into the tubule in the descending loop • Approximately 80% (of the 50% now in the loop) is reabsorbed in the ascending loop • Net excretion = 10% of filtered load
  18. 18. Renal Handling of Urate in Disease Glomerulus Proximal Convoluted Tubule S1 S2 S3 Uric Acid 100% 1-2% 50% 8-12% Inhibition of tubular secretion ▪ Competitive anions Enhanced tubular reabsorption ▪ Dehydration, diuretics, insulin resistance Modulation of OAT expression ▪ Sex hormones, aging, diuretic therapy Mechanisms incompletely defined ▪ Hypertension, hyperparathyroidism, certain drugs and lead nephropathy
  19. 19. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 19
  20. 20. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Course of untreated gout
 
 
 
 
 
 
 
 
 
 
 
 The Course of Untreated Gout
 
 
 
 
 
 
 
 
 
 
 
 The Course of Untreated Gout 21 Acute gout Soft tissue swelling ! (Five years after initial attack, ! 70 percent of patients have no tophi) ! Intercritical gout More frequent attacks, often polyarticular Tophaceous gout ! Chronic gout (50 percent of patients have no !! tophi 10 years after initial attack, ! and 28 percent have no tophi !! after 20 years) Erosion with joint space preservation ! ! Joint space destruction, deformity and tophi that may become confluent (Am Family Physician 1996)
  21. 21. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 25 Acute Gouty Arthritis: Mechanism Hyperuricemia Factors ? Precipitation of urate crystals in joints (e.g., toe, ankle heel, knee, wrist) ! Phagocytosis by Activation of neutrophils Hageman factor ! ! Damage to lysosomes Kinin production, complement activation Lysis of neutrophils Release of Release of crystals lysosomal enzymes ! Acute inflammation (Kelly 2001)
  22. 22. Serum uric acid levels & age 3.0 4.0 5.0 6.0 7.0 8.0 9.0 10.0 11.0 12.0 13.0 Age (years) 10 20 30 40 50 60 Gouty Male Normal Male Gouty Female Normal Female Serum urate levels vary with age and sex. Children: 3 to 4 mg/dl Adult men: 6 to 6.8 mg/dl
  23. 23. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pathology 27 ! • A tophus is a foreign body reaction that includes the MSU crystals surrounded by fibrous tissue.
  24. 24. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Clinical Manifestations 28 • Acute gout: • acute arthritis ..most common manifestation • 80% attacks..monoarticular and lower extremities(MTP’s, ankle and knee). Pain appears last, disappears first. • Differential diagnosis : • septic arthritis, cellulitis or thromboplebitis. • Attacks subside in 3 to 10 days. • Recurrent attacks .. involve more joints and usually persist longer.
  25. 25. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Clinical Manifestations
 29 • Intercritical gout: Asymptomatic period between crises • Duration .. varies, but untreated patients may have a second episode within two years. • Some patients evolve to chronic polyarticular gout without pain free intercritical episodes.
  26. 26. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Clinical Manifestations 30 • Chronic tophaceus Gout: The clinical characteristic is the deposition of solid urate in the connective tissue. • It is associated with early age of onset, long duration of untreated disease, frequent attacks, upper extremity involvement, polyarticular disease and elevated serum uric acid.
  27. 27. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Clinical Manifestations 31 • Transplants with cyclosporine and/or diuretics .. increased risk for tophaceus gout. • Most common sites for tophi : olecranon, prepatellar bursa, ulnar surface and Achilles tendon.
  28. 28. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 32 Hyperuricaemia ⇩ May be asymptomatic ⇩ Deposition of monosodium urate crystals in synovial tissue (contain various Ig’s, complement, fibrinogen, fibronectin) ⇩ Complement activated ⇩ Neutrophils phagocytose & lyse crystals ⇩ Release chemical mediators (e.g. TNF-α; IL-1) ⇩ ACUTE GOUTY ARTHRITIS ⇩ May resolve & become asymptomatic (INTERCRITICAL GOUT)
  29. 29. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 33 Recurrent episodes of Gout ⇩ Large deposits of chalky white urate ! tophi ⇩ Chronic granulomatous inflammatory condition ⇩ Fibrosis of synovium ⇩ Erosion of articular cartilage ⇩ CHRONIC TOPHACEOUS ARTHRITIS ⇩ ankylosis ⇩ Tophi may be deposited in soft tissue ⇩ Can ulcerate if sub-cutaneous
  30. 30. 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 calcium phosphate (radio-opaque) ▫ Contributing factors : hyperuricosuria, low urine output, acidic urine ▫ Urinary alkalinization (pot. Citrate or NaHCO3) ! dissolution of existing stones and prevention of recurrence
  31. 31. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Nephrolithiasis 35 • The prevalence of nephrolithiasis correlates with the serum and urinary uric acid levels. • Serum urate levels 13 mg/dl • Urinary uric acid excretion > 1100 mg/d www.freelivedoctor.com
  32. 32. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Diagnostic Tests 36 • Uric Acid: • normal .. 4.0 to 8.6 mg/dl in men to 3.0 to 5.9 mg/dl in women. • Urinary levels are normal below 750 mg/ 24h. • Urinary levels above 750 mg/dl in 24h in gout or > 1100 mg/dl in asymptomatic hyperuricemia indicates urate overproduction.
  33. 33. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Diagnostic tests 37 • Joint Fluid: Acute gout..inflammatory (>2000 cells/ml); • MSU crystals .. with Polarized light microscope…acute gout..usually intracellular. • MSU crystals do not exclude the possibility of septic arthritis, for this reason it is also recommended to request a Gram smear.
  34. 34. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 38H-E stain (x 100)
  35. 35. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 39 H-E stain (x 400)
  36. 36. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 40
  37. 37. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Diagnostic Tests 41 • 24 urine collection for uric acid determination : • assessing the risk of renal stones and planning for therapy. ! ! • Radiological examination .. to exclude other kinds of arthritis. 24 hour Urinary Uric acid estimation
  38. 38. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Radiologic Features of Gout 42 Appendicular • Tophi • Normal mineralization • Asymmetric polyarticular distribution • Juxta-articular bony erosion associated with periarticular tophi • Overhanging edge of cortex • Punched-out erosions of bone with sclerotic borders (Chapman 1997)
  39. 39. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Radiologic Features of Gout 43 Axial • Non-specific, degenerative changes • Hyperostotic spondylosis or diffuse idiopathic spinal hyperostosis • Disk space narrowing with endplate erosions • Peri-articular erosions
  40. 40. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Differential Diagnosis 44 • Acute Gout: • septic arthritis, pseudogout, Reactive arthritis, acute rheumatic fever and other crystalline arthropathies. • Chronic tophaceus gout: Rheumatoid Arthritis, Pseudogout, Seronegative spondyloarthropathies Erosive osteoarthritis.
  41. 41. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 45
  42. 42. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 46
  43. 43. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 47
  44. 44. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Therapy 48 • Acute Gout: • NSAID’s, corticosteroids or oral colchicine can be used. • NSAID’s are the preferred modality. • When NSAID’s are contraindicated, corticosteroids are effective.
  45. 45. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 49
  46. 46. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Therapy 50 • Intra-articular corticosteroids are an alternative when systemic therapy is contraindicated. • Colchicine has been the medication traditionally used for acute gout, but it has significant GI toxicity and delayed onset of action.
  47. 47. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Therapy 51 • Intercritical Gout: Prevention and prophylaxis.
  48. 48. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Therapy 52 • Diet usually impractical, ineffective and rarely adhered to in clinical practice.
  49. 49. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 53
  50. 50. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 54 Purine nucleotides hypoxanthine xanthine Uric acid Xanthine oxidase Alimentary excretion Urinary excretion Tissue deposition in excess Urate crystal microtophi Phagocytosis with acute inflammation and arthritis uricosurics colchicine NSAID Allopurinol Oxypurinol
  51. 51. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Non-drug Management: 55 Stop diuretics Dietary changes Include: Stop alcohol weight loss
  52. 52. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Dietary advices: 56 Fructose Red meat/sea food. Avoid: Beer Spirits
  53. 53. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 57
  54. 54. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 58
  55. 55. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 59
  56. 56. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 60
  57. 57. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 61
  58. 58. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 62
  59. 59. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 63
  60. 60. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 64
  61. 61. Renal handling of uric acid •glomerular filtration •tubular reabsorption •tubular excretion •post-secretory reabsorption •excretion Drugs That Enhance Excretion of Uric Acid
  62. 62. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 66
  63. 63. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Starting urate -lowering drugs: 67 - Started 1-2 weeks after resolution of the acute attack. - Colchicine or NSAIDs for 3-6 months. Should be treated without interruption of urate- lowering therapy. Urate lowering drugs: Prevention of acute flares during maintenance trt: Flares
  64. 64. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Urate - lowering therapy: 68 Tophi Uric acid stones Indicated in: Recurrent attacks Chronic arthropathy
  65. 65. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 69
  66. 66. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Uricosuric agents 70 ❖ Probenecid, sulfinpyrazone,benzbromarone ❖ Can be used as second-line therapy for patients with underexcretion of uric acid. ❖ Fluid intake should be increased/ urine pH maintained above 6 to prevent development of uric acid stones. ❖ Benzbromarone, a powerful uricosuric drug, is more active than allopurinol taken at the maximum allowed dose for patients with moderate renal failure. ❖ Hepatotoxic.
  67. 67. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Uricosuric therapy 71 • Probenecid • blocks tubular reabsorption of uric acid • enhances urine uric acid excretion • increases urine uric acid level • decreases serum uric acid level
  68. 68. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Why Alkaline Urine 72 ■ Uric acid is more soluble in urine than in water. ■ The pH of urine greatly influences its solubility. ■ pH 5 urine is saturated with uric acid at concentrations ranging from 6 to 15 mg/ dl. ■ At pH 7 saturation is reached at concentration between 158 and 200mg/ dl
  69. 69. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Uricosuric therapy 73 • moderately effective • increases risk of nephrolithiasis • not used in patients with renal disease • frequent, but mild, side effects • some drugs reduce efficacy (e.g., aspirin)
  70. 70. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Choosing a urate-lowering drug 74 hyperuricemia excessive production inadequate excretion xanthine oxidase inhibitor uricosuric agent
  71. 71. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Therapy …...ALLOPURINOL 75 • Allopurinol decreases uric acid in overproducers and underexcreters; it is also indicated in patients with a history of urolithiasis, tophaceus gout, renal insufficiency and in prophylaxis of tumor lysis syndrome.
  72. 72. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 76
  73. 73. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Urate-lowering drugs: Febuxostat 77 ❖ XOI ❖ 80-120 mg/ day are more effective than allopurinol 300 mg/day. ❖ Dose adjustment is not necessary in mild renal failure. ❖ Side-effects: raised liver enzyme activity ;serious cardiovascular events, precludes use in patients with ischaemic or CHF.
  74. 74. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 78
  75. 75. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 79
  76. 76. Case presentation - therapy NSAID steroid colchicine (low-dose) allopurinol NSAID days 1-10 days 11-365 days 365+
  77. 77. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 81 Management of Acute Gout
  78. 78. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 82 Management of Recurrent Gout
  79. 79. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Surgical intervention: 83 Last resort for gouty arthritis Removal of tophi Joint fusion Joint replacement ! Ulceration of tophi : debridement, dressing with sodium bicarbonate solution ! Indications for chronic tophaceous gout : Advanced tophi deposition resulting in major joint destruction Loss of involved joint movements a/w severe pain Tophi collection causing pressure symptoms, eg carpal tunnel syndrome of wrist Tophaceous ulcer Cosmetic eg ear lobe tophi
  80. 80. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS TOPHI 
 CARPAL TUNNEL SYNDROME Dr.Sandeep Agrawal,Gondia
  81. 81. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS TOPHI FOOT
  82. 82. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 86
  83. 83. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Gout knee
  84. 84. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS GOUT
 HIP:ILIOPSOAS BURSITIS
  85. 85. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 89
  86. 86. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 90 Olecranon Bursitis
  87. 87. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 91
  88. 88. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 92
  89. 89. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Summary 93 • Tophaceous deposits related to the duration and degree of hyperuricemia (A.F.P. 1996) • Medication playing a role potentially avoiding the need for surgery • X-rays- nonspecific but CT or MRI documented for the localizing biopsy and suggestive diagnosis
  90. 90. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Take Home Message 94
  91. 91. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 95
  92. 92. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Gout or pseudogout? 96 Gout ● >40 ● small joints esp 1st MTP ● Severe joint pain swelling ! ● Uric acid crystals neg bifringent ● Rest, nsiad prohylaxis ● hyperuricaemia Pseudogout Elderly Large joints esp knee ! Mod pain and swelling ! ! Calcium pyrophosphate positively bifringent Rest, nsaid, joint aspiration
  93. 93. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS PSEUDOGOUT 97 • Calcium pyrophosphate Crystal Deposition Disease (CPPD) is the syndrome secondary to the calcium pyrophosphate in articular tissues. • Includes: • Chondrocalcinosis • Chronic CPPD • Pseudogout.
  94. 94. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 98 • Etiology:Unknown secondary to changes in the cartilage matrix or secondary to elevated levels of calcium or inorganic pyrophosphate. • Pathology: CPPD crystals .. in joint capsule and fibrocartilaginous structures. • Neutrophil infiltration and erosions.
  95. 95. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 99 • Demographics: Predominantly elderly, peak age 65 to 75 years old Female predominance (F:M, 2-7:1). • Prevalence.. 5 to 8%
  96. 96. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 100 • Disease Associations: • hyperthyroidsm, hypocalciuria, hypercalcemia, hemochromatosis, hemosiderosis, hypophosphatasia, hypomagnesemia, hypothyroidsm, gout, neuropathic joints, amyloidosis, trauma and OA.
  97. 97. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 101 • Clinical Manifestations • Pseudogout: Acute self-limited attacks resembling acute gout. knee is involved in 50% of cases, followed by the wrist, shoulder, ankle, and elbow.
  98. 98. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 102 • In 5% of patients gout can coexist with pseudogout. • Diagnosis is confirmed with synovial fluid analysis and/or the presence of chondrocalcinosis in the radiographs. • Acute Pseudogout primarily affects men.
  99. 99. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Psedogout 103 • Chronic CPPD: • predominately affects women; • Progressive, often symmetric, polyarthritis. • Usually affects the knees, wrists, 2nd and 3rd MCP’s, hips, spine, shoulders, elbows and ankles. • Chronic CPPD differs from pseudogout in its chronicity, involvement of the spine and MCP’s.
  100. 100. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 104
  101. 101. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 105 • Chondrocalcinosis: Generally is an incidental finding in XRays. • Diagnostic Tests: Inflammatory cell count in the synovial fluid. Rhomboidal or rodlike intracellular crystals. Imaging studies reveal chondrocalcinosis usually in the knee, but can be seen in the radial joint, symphisis pubis and intervertebral discs.
  102. 102. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 106 • Differential Diagnosis: Includes septic arthritis, gout, inflammatory OA, Rheumatoid Arthritis, neuropathic arthritis and Hypertrofic Osteoarthropathy.
  103. 103. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Chondrocalcinosis: knee 
 
 Calcification of the menisci and articular cartilage that is typical of chondrocalcinosis. 
 Calcification is due to focal deposits of calcium pyrophosphate dihydrate crystals in articular cartilage.
 
 Classically, both knees (especially menisci) are involved, and the calcifications, although linear, are not smooth and continuous but are interrupted by multiple focal deposits.
 
 Statistically, the knee is the most frequent site of such calcification and attacks of pseudogout. However, other joints may be involved.
 Many patients with chondrocalcinosis on radiograph have not had clinical attacks of pseudogout, and some patients with proven attacks of pseudogout do not have radiographic evidence of chondrocalcinosis on routine radiographs. 
 

  104. 104. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Syndromes Associated with Hydroxyapatite 108 • Acute monoarthritis (pseudopseudogout) • Acute calcific tendinitis, bursitis • Scleroderma, dermatomyositis • Heterotopic calcification • Milwaukee shoulder • Crowned Dens Syndrome
  105. 105. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Acute Apatite Monoarthritis
 (Pseudopseudogout) 109 • Is usually a peri-arthritis. • Intense inflammation (looks septic) • Synovial fluid often non-inflammatory. • Often causes podagra (especially in younger women). • Look for the telltale calcifications on radiographs.
  106. 106. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 110
  107. 107. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Milwaukee Shoulder 111 • Severe, destructive shoulder arthropathy. • Seen in elderly females with DJD of shoulder. • High-riding humeral head on radiographs (large rotator cuff tear). • Non-inflammatory fluid with BCP crystals.
  108. 108. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Crowned dens syndrome 112 • Is an association of acute cervical pain and calcifications in the peri-odontoid space. • This disease affects only adult females. • Patients present with inflammatory signs, can be treated with non-steroid anti-inflammatory drugs and recover without sequela. • CPPD deposition can also lead to this syndrome. • Radiologically - crowned dens.
  109. 109. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 113
  110. 110. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS Pseudogout 114 • Therapy: It is similar to gout and includes intrarticular corticosteroids. Colchicine can be used in acute attacks and also in prophylaxis. There is no specific treatment for chronic CPPD. It is important to treat secondary causes and colchicine could be helpful.
  111. 111. DISCLAMER 115 .This presentation is prepared for doctors in general. . Some graphics and jpeg files are taken from Google Image and Whatsapp to heighten the specific points in this presentation.  • If there is any objection/or copyright violation, please inform drsandeep123@gmail.com for prompt deletion.  • It is intended for use only by the doctors of orthopaedic surgery. . Views expressed in this presentation are personal. • .For any confusion please contact the sole author for clarification.  • Every body is allowed to copy or download and use the material best suited to him.  There is no financial involvement.  • For any correction or suggestion please contact drsandeep123@gmail.com.

×