1. GOUTSymptoms,Control,Diet & TreatmentDr.Sandeep AgrawalMS,DNB (ORTHOPAEDICS)Agrasen HospitalGondiaMaharashtraGOUTPSEUDOGOUINDIATdrsandeep123@gmail.com09960122234Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS

2. Introduction:Purine metabolismManagementDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS2IntroductionDiagnosisComplicationsGOUT 3. Gout is a syndrome caused by the inflammatory response to tissuedeposition of monosodium urate crystals (MSU).Uric acid has1. Low water solubility.2 . Especially in low pHBlood levels high. precipitates . deposit as sodiumurate crystals on joints, kidneys and subcutaneoustissue( tophi)Uric acid can accumulate due to:Overproduction of purine nucleotidesEnhanced cell turnover (purine degradation)Decreased in purine salvage pathwayUnderexcretion of uric acid 4. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS4 5. Gout: pathophysiologyOverproduction Under excretionDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS5Food intake Cell breakdownPurinesUric acidHYPERURICAEMIAKidney Soft tissue ofthe jointsOther tissueEar 6. Click to edit Master title styleDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS6Historical ReviewPodagra (Greek Pous), gout (Latin Gutta), honoured in antiquityHippocrates (460-370 B.C.): the unwalkable diseaseScheele, 1776: uric acid in urineWollaston, 1797: ear tophusGarrod, 1848: uric acid in bloodTalbot, 1967, quoted famous patients: Darwin,Harvey, Hunter, Newton and sydenhamHuber, 1896: x-ray characteristics of gouty arthritis(Clin. Radiol. 1975) 7. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS7Introduction Hyperuricemia: at 37C, value of urate saturationabout 7 mg/dl; 2.3 to 17.6 % ofthe populations Natural Hx of gout: 4 stagesa. asymptomatic hyperuricemiab. acute gouty arthritis: MSU crystal deposition;4th to 6th decades; great toe, ankle,heel, knee, wrist, finger, and elbowin order of frequency.c. intercritical goutd.chronic tophaceous gout: aggregates of MSUcrystals in and around joints 8. Precipitating Risk FactorsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS8 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. Interrelationships (HU, CRD, CVD)CELLPURINEXOURIC ACIDSMC ProliferationHYPERURICEMIAVasoconstrictionRAS ActivationCOX2 ActivationHYPERTENSIONENDOTHELIAL DYSFUNCTION& CARDIOVASCULAR DISEASERENAL DISEASE PROGRESSIONTissue HypoxiaCell DeathInsulin Resistance 10. HyperuricemiaDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS10hyperuricemia results when production exceeds excretion 11. HyperuricemiaDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS11net uric acid loss results when excretion exceeds production 12. excessiveproductionDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS12inadequateexcretionhyperuricemia 13. Hyperuricemia Mechanismoverproducers underexcretorsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS13hyperuricemia 14. Urate-lowering drugsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS14net reduction in total body pool ofuric acidblockproductionenhanceexcretion 15. Classifying hyperuricemiaDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS15 serum uric acid level urine uric acid excretion (24-hour) 16. Gout: Pathophysiology Uric acid: overproduction vs. underexcretion Mechanisms of urate productioncellular nucleoproteins/nucleotides (~ 66%)diet (~33%) Mechanisms of urate excretionkidney (~66%)gut (~33%) 17. Renal Handling of Uric Acid Completely filtered by the glomerulus Completely (essentially) reabsorbedin the proximal tubule Approximately 50% is secreted backinto the tubule in the descending loop Approximately 80% (of the 50% nowin the loop) is reabsorbed in theascending loop Net excretion = 10% of filtered loadDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS17 18. Renal Handling of Urate in DiseaseGlomerulusProximalConvolutedTubuleS1S2S3Uric Acid100%1-2%50%8-12% Inhibition of tubular secretionCompetitive anions Enhanced tubular reabsorptionDehydration, diuretics, insulinresistance Modulation of OAT expressionSex hormones, aging, diuretictherapy Mechanisms incompletely definedHypertension, hyperparathyroidism,certain drugs and lead nephropathy 19. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS19 20. The Course of Untreated GoutThe Course of Untreated GoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS21Acute gout Soft tissue swelling(Five years after initial attack,70 percent of patients have no tophi)Intercritical gout More frequent attacks, oftenpolyarticularTophaceous goutChronic gout (50 percent of patients have notophi 10 years after initial attack,and 28 percent have no tophiafter 20 years)Erosion with joint space preservationJoint space destruction, deformity and tophi thatmay become confluent(Am Family Physician 1996) 21. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS25Acute Gouty Arthritis: MechanismHyperuricemiaFactors ?Precipitation of urate crystals in joints(e.g., toe, ankle heel, knee, wrist)Phagocytosis by Activation ofneutrophils Hageman factorDamage to lysosomes Kinin production,complement activationLysis of neutrophilsRelease of Release ofcrystals lysosomal enzymesAcute inflammation(Kelly 2001) 22. Serum uric acid levels & age13.012.011.010.09.08.07.06.05.04.03.010 20 30 40 50 60Age (years)Gouty MaleNormal MaleGouty FemaleNormal FemaleSerum urate levels vary with age and sex.Children: 3 to 4 mg/dlAdult men: 6 to 6.8 mg/dl 23. PathologyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS27 A tophus is a foreign body reaction thatincludes the MSU crystals surrounded byfibrous tissue. 24. Clinical ManifestationsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS28 Acute gout: acute arthritis ..most commonmanifestation 80% attacks..monoarticular and lowerextremities(MTPs, ankle and knee). Pain appears last, disappears first. Differential diagnosis : septic arthritis, cellulitis orthromboplebitis. Attacks subside in 3 to 10 days. Recurrent attacks .. involve more joints andusually persist longer. 25. Clinical ManifestationsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS29 Intercritical gout: Asymptomatic periodbetween crises Duration .. varies, but untreatedpatients may have a second episodewithin two years. Some patients evolve to chronicpolyarticular gout without pain freeintercritical episodes. 26. Clinical ManifestationsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS30 Chronic tophaceus Gout: The clinicalcharacteristic is the deposition of solidurate in the connective tissue. It is associated with early age of onset,long duration of untreated disease,frequent attacks, upper extremityinvolvement, polyarticular disease andelevated serum uric acid. 27. Clinical ManifestationsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS31 Transplants with cyclosporine and/ordiuretics .. increased risk for tophaceusgout. Most common sites for tophi :olecranon, prepatellar bursa, ulnarsurface and Achilles tendon. 28. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS32HyperuricaemiaMay be asymptomaticDeposition of monosodium urate crystals in synovial tissue(contain various Igs, complement, fibrinogen, fibronectin)Complement activatedNeutrophils phagocytose & lyse crystalsRelease chemical mediators (e.g. TNF-; IL-1)ACUTE GOUTY ARTHRITISMay resolve & become asymptomatic(INTERCRITICAL GOUT) 29. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS33Recurrent episodes of GoutLarge deposits of chalky white urate tophiChronic granulomatous inflammatory conditionFibrosis of synoviumErosion of articular cartilageCHRONIC TOPHACEOUS ARTHRITISankylosisTophi may be deposited in soft tissueCan ulcerate if sub-cutaneous 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 calciumphosphate (radio-opaque) Contributing factors : hyperuricosuria, low urine output, acidicurine Urinary alkalinization (pot. Citrate or NaHCO3) dissolution of existing stones and prevention of recurrence 31. NephrolithiasisDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS35 The prevalence of nephrolithiasiscorrelates with the serum andurinary uric acid levels. Serum urate levels 13 mg/dl Urinary uric acid excretion > 1100mg/dwww.freelivedoctor.com 32. Diagnostic Tests Uric Acid: normal .. 4.0 to 8.6 mg/dl in men to 3.0Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS36to 5.9 mg/dl in women. Urinary levels are normal below 750mg/ 24h. Urinary levels above 750 mg/dl in 24h ingout or > 1100 mg/dl in asymptomatichyperuricemia indicates urateoverproduction. 33. Diagnostic testsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS37 Joint Fluid: Acute gout..inflammatory(>2000 cells/ml); MSU crystals .. with Polarized lightmicroscopeacute gout..usuallyintracellular. MSU crystals do not exclude thepossibility of septic arthritis, for thisreason it is also recommended torequest a Gram smear. 34. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS38H-E stain (x 100) 35. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS39H-E stain (x 400) 36. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS40 37. Diagnostic Tests24 hour Urinary Uric acid estimationDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS41 24 urine collection for uric aciddetermination : assessing the risk of renal stones andplanning for therapy. Radiological examination .. to excludeother kinds of arthritis. 38. Radiologic Features of GoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS42Appendicular Tophi Normal mineralization Asymmetric polyarticulardistribution Juxta-articular bony erosionassociated with periarticular tophi Overhanging edge of cortex Punched-out erosions of bone withsclerotic borders (Chapman 1997) 39. Radiologic Features of GoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS43Axial Non-specific, degenerative changes Hyperostotic spondylosis or diffuse idiopathicspinal hyperostosis Disk space narrowing with endplate erosions Peri-articular erosions 40. Differential DiagnosisDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS44 Acute Gout: septic arthritis, pseudogout, Reactivearthritis, acute rheumatic fever andother crystalline arthropathies. Chronic tophaceus gout:Rheumatoid Arthritis, Pseudogout,Seronegative spondyloarthropathiesErosive osteoarthritis. 41. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS45 42. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS46 43. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS47 44. TherapyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS48 Acute Gout: NSAIDs, corticosteroids or oralcolchicine can be used. NSAIDs are the preferred modality. When NSAIDs are contraindicated,corticosteroids are effective. 45. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS49 46. TherapyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS50 Intra-articular corticosteroids are analternative when systemic therapy iscontraindicated. Colchicine has been the medicationtraditionally used for acute gout, but ithas significant GI toxicity and delayedonset of action. 47. TherapyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS51 Intercritical Gout:Prevention and prophylaxis. 48. TherapyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS52 Dietusually impractical, ineffective andrarely adhered to in clinical practice. 49. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS53 50. AllopurinolDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS54Purine nucleotideshypoxanthinexanthineUric acidXanthineoxidaseAlimentaryexcretionUrinaryexcretionOxypurinolTissue deposition inexcessUrate crystal microtophiPhagocytosiswith acuteinflammationand arthritisuricosuricscolchicine NSAID 51. Non-drug Management:Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS55Stop diureticsDietary changesInclude:Stop alcohol weight loss 52. Dietary advices:Avoid:Beer SpiritsDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS56FructoseRed meat/sea food. 53. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS57 54. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS58 55. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS59 56. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS60 57. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS61 58. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS62 59. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS63 60. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS64 61. Renal handling of uric acidglomerular filtrationtubular reabsorptiontubular excretionpost-secretoryreabsorptionexcretionDrugs That Enhance Excretion of Uric Acid 62. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS66 63. Starting urate -lowering drugs:Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS67- Started 1-2 weeks after resolution of the acute attack.- Colchicine or NSAIDs for 3-6 months.Should be treated without interruption of urate-loweringtherapy.Urate lowering drugs:Prevention of acute flares during maintenance trt:Flares 64. Urate - lowering therapy:Indicated in:Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS68TophiUric acid stonesRecurrent attacksChronic arthropathy 65. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS69 66. Uricosuric agentsProbenecid, sulfinpyrazone,benzbromaroneCan be used as second-line therapy for patients withunderexcretion of uric acid.Fluid intake should be increased/ urine pH maintainedabove 6 to prevent development of uric acid stones.Benzbromarone, a powerful uricosuric drug, is more activethan allopurinol taken at the maximum allowed dose forpatients with moderate renal failure.Hepatotoxic.Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS70 67. Uricosuric therapyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS71 Probenecid blocks tubular reabsorption ofuric acid enhances urine uric acidexcretion increases urine uric acid level decreases serum uric acid level 68. Why Alkaline UrineDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS72 Uric acid is more soluble in urine than inwater. The pH of urine greatly influences itssolubility. pH 5 urine is saturated with uric acid atconcentrations ranging from 6 to 15mg/dl. At pH 7 saturation is reached atconcentration between 158 and 200mg/dl 69. Uricosuric therapyDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS73 moderately effective increases risk of nephrolithiasis not used in patients with renaldisease frequent, but mild, side effects some drugs reduce efficacy(e.g., aspirin) 70. Choosing a urate-lowering drugexcessiveproductionDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS74inadequateexcretionhyperuricemiaxanthine oxidaseinhibitor uricosuric agent 71. Therapy ...ALLOPURINOLDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS75 Allopurinol decreases uric acid inoverproducers and underexcreters; it isalso indicated in patients with a historyof urolithiasis, tophaceus gout, renalinsufficiency and in prophylaxis of tumorlysis syndrome. 72. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS76 73. Urate-lowering drugs: Febuxostat XOI80-120 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.Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS77 74. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS78 75. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS79 76. Case presentation - therapyNSAIDsteroidcolchicine (low-dose)allopurinolNSAIDdays 1-10 days 11-365 days 365+ 77. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS81Management of Acute Gout 78. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS82Management of Recurrent Gout 79. Surgical intervention:Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS83Last resort for gouty arthritisRemoval of tophiJoint fusionJoint replacementUlceration of tophi : debridement, dressing with sodium bicarbonate solutionIndications for chronic tophaceous gout :Advanced tophi deposition resulting in major joint destructionLoss of involved joint movements a/w severe painTophi collection causing pressure symptoms, eg carpal tunnel syndrome of wristTophaceous ulcerCosmetic eg ear lobe tophi 80. TOPHICARPAL TUNNEL SYNDROMEDr.Sandeep Agrawal,Agrasen Hospital,Gondia MSDr.SandeepAgrawal,Gondia 81. TOPHI FOOTDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 82. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS86 83. Gout kneeDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 84. GOUTHIP:ILIOPSOAS BURSITISDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 85. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS89 86. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS90Olecranon Bursitis 87. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS91 88. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS92 89. SummaryDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS93 Tophaceous deposits related to the durationand degree of hyperuricemia (A.F.P. 1996) Medication playing a role potentially avoidingthe need for surgery X-rays- nonspecific but CT or MRI documentedfor the localizing biopsy and suggestivediagnosis 90. Take Home MessageDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS94 91. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS95 92. Gout or pseudogout?PseudogoutElderlyLarge joints esp kneeMod pain and swellingDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS96Gout >40 small joints esp 1st MTP Severe joint pain swelling Uric acid crystals neg bifringent Rest, nsiad prohylaxis hyperuricaemiaCalcium pyrophosphatepositively bifringentRest, nsaid, jointaspiration 93. PSEUDOGOUTDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS97 Calcium pyrophosphate CrystalDeposition Disease (CPPD) is thesyndrome secondary to the calciumpyrophosphate in articular tissues. Includes: Chondrocalcinosis Chronic CPPD Pseudogout. 94. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS98 Etiology:Unknownsecondary to changes in the cartilagematrix or secondary to elevated levels ofcalcium or inorganic pyrophosphate. Pathology:CPPD crystals .. in joint capsule andfibrocartilaginous structures. Neutrophil infiltration and erosions. 95. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS99 Demographics: Predominantly elderly,peak age 65 to 75 years oldFemale predominance (F:M, 2-7:1). Prevalence.. 5 to 8% 96. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS100 Disease Associations: hyperthyroidsm, hypocalciuria,hypercalcemia, hemochromatosis,hemosiderosis, hypophosphatasia,hypomagnesemia, hypothyroidsm, gout,neuropathic joints, amyloidosis, traumaand OA. 97. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS101 Clinical Manifestations Pseudogout:Acute self-limited attacks resemblingacute gout.knee is involved in 50% of cases,followed by the wrist, shoulder, ankle,and elbow. 98. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS102 In 5% of patients gout can coexist withpseudogout. Diagnosis is confirmed with synovial fluidanalysis and/or the presence ofchondrocalcinosis in the radiographs. Acute Pseudogout primarily affects men. 99. PsedogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS103 Chronic CPPD: predominately affects women; Progressive, often symmetric, polyarthritis. Usually affects the knees, wrists, 2nd and 3rd MCPs,hips, spine, shoulders, elbows and ankles. Chronic CPPD differs from pseudogout in itschronicity, involvement of the spine and MCPs. 100. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS104 101. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS105 Chondrocalcinosis: Generally is anincidental finding in XRays. Diagnostic Tests: Inflammatory cellcount in the synovial fluid. Rhomboidalor rodlike intracellular crystals. Imagingstudies reveal chondrocalcinosis usuallyin the knee, but can be seen in theradial joint, symphisis pubis andintervertebral discs. 102. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS106 Differential Diagnosis: Includes septicarthritis, gout, inflammatory OA,Rheumatoid Arthritis, neuropathicarthritis and HypertroficOsteoarthropathy. 103. Chondrocalcinosis: kneeCalcification of the menisci and articular cartilage that is typical ofchondrocalcinosis.Calcification is due to focal deposits of calcium pyrophosphate dihydratecrystals in articular cartilage.Classically, both knees (especially menisci) are involved, and thecalcifications, although linear, are not smooth and continuous but areinterrupted by multiple focal deposits.Statistically, the knee is the most frequent site of such calcification andattacks of pseudogout. However, other joints may be involved.Many patients with chondrocalcinosis on radiograph have not had clinicalattacks of pseudogout, and some patients with proven attacks of pseudogoutdo not have radiographic evidence of chondrocalcinosis on routine radiographs.Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS 104. Syndromes Associated withHydroxyapatite Acute monoarthritis (pseudopseudogout) Acute calcific tendinitis, bursitis Scleroderma, dermatomyositis Heterotopic calcification Milwaukee shoulder Crowned Dens SyndromeDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS108 105. Acute Apatite Monoarthritis(Pseudopseudogout)Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS109 Is usually a peri-arthritis. Intense inflammation (looks septic) Synovial fluid often non-inflammatory. Often causes podagra (especially inyounger women). Look for the telltale calcifications onradiographs. 106. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS110 107. Milwaukee Shoulder Severe, destructive shoulder arthropathy. Seen in elderly females with DJD ofshoulder. High-riding humeral head on radiographs(large rotator cuff tear). Non-inflammatory fluid with BCP crystals.Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS111 108. Crowned dens syndromeDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS112 Is an association of acute cervical pain andcalcifications in the peri-odontoid space. This disease affects only adult females. Patients present with inflammatory signs, canbe treated with non-steroid anti-inflammatorydrugs and recover without sequela. CPPD deposition can also lead to thissyndrome. Radiologically - crowned dens. 109. Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS113 110. PseudogoutDr.Sandeep Agrawal,Agrasen Hospital,Gondia MS114 Therapy: It is similar to gout andincludes intrarticular corticosteroids.Colchicine can be used in acute attacksand also in prophylaxis. There is nospecific treatment for chronic CPPD. It isimportant to treat secondary causes andcolchicine could be helpful. 111. DISCLAMER115.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. 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