Crystal arthritis ugs

overview of crystal arthritis

1. CRYSTAL ARTHRITIS Dr. M Kasi Viswanadham PG in Orthopaedics

2. GOUT word Gout is derived from the latin word ‘ gutta ’ means drop. based on the ancient belief that the arthritis is due to deposition of malevolent humor by evil spirits into the joint, drop by drop

3. Gout is a disorder of purine metabolism characterized by hyperuricaemia , deposition of monosodium urate monohydrate crystals in joints and peri-articular tissues and recurrent attacks of acute synovitis . Late changes include cartilage degeneration, renal dysfunction and uric acid urolithiasis .

4. 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 Galen described the tophi . Crystals in gouty tophi was first demonstrated by Antony Van Leeuwenhoek in (1679 ) Sir Alfred Garrod demonstrated hyperuricemia as the basic cause of gout(1848) McCarty and Hollander established the association between gouty arthritis and articular crystal deposition(1961)

5. Gout is much more common in men than in women; rare before menopause and more common in old age Male ,female ratio 2.7:1

6. pathogenesis The pathogenesis of gout depends on three vital steps: (1) the development of hyperuricaemia ; (2) the formation of monosodium urate monohydrate ( urate ) crystals; (3) the interaction between the urate crystals and the inflammatory system.

7. This disorder can be progressive through four stages if undertreated 1. Asymptomatic hyperuricemia 2. Acute gout 3. Intercritical gout 4. Chronic tophaceous gout

8. Asymptomatic hyperurecemia Asymptomatic Serum uric acid levels-more than 6mg/dl risk of gout increases with the degree and duration of hyperuricaemia .

9. Acute gout most common early clinical manifestation Usually, only one joint is affected initially, but polyarticular acute gout can occur in subsequent episodes Factors provking manifestations-. alcohol, obesity abrupt change in serum uric acid concentration Diuretic use, hypertension, renal insufficiency, and osteoarthritis

10. Most acute attacks of gout involve a single joint in the lower limb, most commonly the first metatarso phalangeal joint also referred to as podagra . Others-ankle, heel, knee, wrist, fingers, and elbow joints

11. Symptoms-severe pain, Swelling Erythema Warmth Tenderness Low grade fever Starts during night peak 1-2 days.last for 7-10 days Differential diagnosis-septic arthritis,cellulitis

12. Acute gout

13. Intercritical gout intercritical period is the time between the acute attacks; the term prophylactic period has been preferred because its emphasizes the value of medication which inhibits or prevents recurring acute episodes.

14. Chronic tophius gout Massive deposition of monosodium urate crystal( tophi ) in the articular cartilage, subchondral bone, synovial membrane, capsular, periarticular tissue and tendon sheaths. Occurs late (an avg 12 yrs)after intial attack

15. Chronic gout

16. Tophaceous nodule consist of multicentric deposition of urate crystal ,inter cellular matrix and foreign body grannulomatous reaction. Tophi firm yellow in colour occsionally discharge cheesy or chalky white material.

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19. Complications of tophi gout- pain,soft tissue damage and deformity,joint destruction, nerve compression syndromes

20. Renal manifestation of gout Nephrolithiasis Acte gouty nephropathy Chronic gouty nephropathy

21. diagnosis

22. Base line lab tests-urine analysis renal function tests Serum urate - normal value is 6-7 mg/dl (6.8mg/dl)  an elevated serum uric acid level does not indicate or predict gout   hyperuricemia in the absence of symptoms is not diagnostic of gout.   diagnosed based on the discovery of urate crystals in the synovial fluid or soft tissues. 

23. radiography Early in the disease, radiographs are often normal or show only soft-tissue swelling Radiographic findings characteristic of gout, which generally do not appear within the first year of disease onset

24. Asymmetrical Punched out erosion Lytic lesions Overhanging edges Scleorotic borders Differ from rhematoid arthrits Maintenance of the joint space Absence of periarticular osteopenia Location outside the joint capsule

25. identification of urate crystals the gold standard for conformation of the diagnosis identification of urate crystals in synovial fuid using polarized light microscopy is highly specific for gout . examined with a polarizing filter, they are yellow when aligned parallel to the slow axis of the red compensator, but they turn blue when aligned across the direction of polarization ( ie , they exhibit negative birefringence).

26. Histology Sample send in 100% alcohol

27. ultrasound A "double contour" sign , consisting of a hyperechoic , irregular line of monosodium urate crystals on the surface articular cartilage overlying an adjacent hyperechoic bony contour "Wet clumps of sugar ," representing tophaceous material, described as hyperechoic and hypoechoic heterogeneous material with an anechoic rim Bony erosions adjacent to tophaceous deposits

28. Differential diagnosis acute gout= infective (septic) arthritis; traumatic synovitis ; palindromic rheumatism seronegativspond-arthritides Rhematic fever

29. d Differential diagnosis of chronic gout nodular rheumatoid arthritis; osteoarthritis with Heberden’s / Bouchard’snodes ;

30. Management

31. Treatment The acute attack Resting the joint Applying ice packs if pain is severe, NSAIDs Colchicine (may cause diarrhoea , nausea and vomiting) A tense joint effusion may require aspiration and intra- articular injection of corticosteroids. Oral corticosteroids. The sooner treatment is started the sooner is the attack likely to end.

32. Interval therapy Between attacks, attention should be given to simple measures such as losing weight cutting out alcohol and Eliminating diuretics.

33. Chronic gout Uricosuric drugs ( probenecid or sulfinpyrazone ) can be used if renal function is normal. Allopurinol a xanthine oxidase inhibitor, is usually preferred for patients with renal complications or chronic tophaceous gout allopurinol is definitely the drug of choice

34. Urate -lowering drugs should never be started before the acute attack has completely subsided , and they should always be covered by an anti- inflammatory preparation or colchicine , otherwise they may actually prolong or precipitate an acute attack.

35. Surgery Ulcerating tophi that fail to heal with conservative treatment can be evacuated by curettage the wound is left open and dressings are applied until it heals.

36. Calcium pyrophosphate dihydrate (CPPD) crystal associated arthropathies idiopathic presents as sporadic episodes in the majority of patient rare familial forms The autosomal dominant form of the disease has been shown to be related to a mutation in the ANKH gene, which encodes a transmembrane inorganic pyrophosphate transport channel

37. association with some metabolic disorders- hyperparathyroidism, haemochromatosis , hypophosphatasia , Wilson’s disease, ochronosis , hypo- calciuric hypercalcaemia diabetes mellitus hypomagnasaemia intra- articular injections of hyaluronic acid preparations (such as Hylan GF-20) may trigger acute attack of pseudogout

38. o Age is most important risk factor Osteoarthritis (OA) - threefold increased risk if CPPD present Previous joint trauma/injury Joint surgery/ lavage promotes crystal shedding

39. Incidence and prevalence uncertain Strong association with age prevalence 3.7% in age 55-59 17% in age 80-84% CPPD associated arthritis is third most common inflammatory arthritis most common acute mono- articular arthritis in elderly ; typically involves the knee

40. pathogenesis Not known Disorder of articular cartilage with altered chondrocyte cartilage matrix abnormalities,altered activity of enzymes that produces pyrophoshates which combines with calcium ions to form CPPD crystals

41. The deposits are often visible as a fine layer of calcification overlying the menisci and articular cartilage of the knee- termed chondrocalcinosis

42. The crystals may provoke an acute attack of synovitis - referred to as pseudo-gout. Pseudo gout Clinical syndrome of acute synovitis with intraarticular (IA) Calcium pyrophosphate dehydrate (CPP) crystal deposition o Most common joints knee and wrist

43. Chronic form referred to as calcium pyrophosphate deposition (CPPD) Arthropathy Increases development of osteoarthritis

44. Chondrocalcinosis Asymptomatic Incidental finding

45. Pseudogout is the most common form presents as acute episodes of synovitis at a single joint, most often at the knee . More common in men, the ‘attack’ typically lasts from a few days to 3-4 weeks characterised by acute pain, swelling and warmth at the affected joint, often indistinguishable from gout.

46. Chronic CPPD: predominately affects women; it is a 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.

47. Radiograph of involved joint Chondrocalcinosis (CC) = linear densities in joints; best seen on films of pelvis, hand and knee Only detects 40% articular CPPD disease Subchondral cysts Aggressive joint degeneration; osteophyte formation

48. Arthrocentesis Inflammatory Synovial Aspirate: mean leukocyte count of 24,000 cells/ μ L with neutrophil predominance Gram stain and culture necessary to rule out infectious arthritis Screening for metabolic disorders

49. Gold standard: synovial fluid analysis under polarized light microscopy with rhomboid crystals, absent/weak positive birefringence polarizing filter CPP crystals change color depending upon their alignment relative to the direction of the red compensator. They are positively birefringent , appearing blue when aligned parallel with the slow axis of the compensator and yellow when perpendicular. The sensitivity of a synovial fluid analysis for crystals is 84%, with a specificity of 100%. 

50. Ultrasound – CPPD in peripheral joints appears as punctuate pattern with thin hyperechoic deposits Specificity 86.7%, Sensitivity 96.4%; Sensitivity varies with joint Most accurate in mild cartilage degeneration MRI - insensitive for articular CPPD CT – sensitive for CPPD; however not specific

51. Differential diagnosis o Gout - negative birefringent monosodium urate crystals; elevated uric acid; first attack usually in foot o OA: may be associated with CPPD; chronic symptoms o RA : positive serology (Rheumatoid factor, Anti- citrullinated peptide antibody) and elevated acute phase reactants; morning stiffness; polyarticular ; symmetric arthritis of wrist, hand or finger joints; rheumatoid nodules; Symptoms >6 weeks Septic Arthritis : SF analysis with turbidity, >10,000 PMNs low glucose and elevated lactic acid; positive Gram stain and culture o Trauma

52. treatment- o Ice o Rest o Joint aspiration o Intraarticular glucocorticosteroids o Oral Nsaids o Cyclooxygenase-2 selective agents o Colchicine o Parenteral Adrenocorticotropic Hormone

53. Prognosis 1. Acute attacks self-limited, resolve 7-10 days 2. Progressive joint damage; destructive arthropathy resembling neuropathic(Charcot’s) joints 3. Large joint arthropathy may require joint replacement

54. II. Basic calcium phosphate hydroxy-apatite (BCP) crystal associated arthropathies : The BCP crystals includes- hydroxy -apatite, octacalcium Phosphate and tricalcium phosphate Manifestations - Periarthritis / tendonitis Milwaukee shoulder syndrome (MSS) Osteoarthritis Erosive arthritis

55. Milwaki shoulder syndrome more common in women affects a single joint- most often the shoulder, or the knee. there may be a history of preceding trauma or overuse of the joint. There are marked degenerative changes on radiology, with the presence of loose bodies and calcification BCP crystals is difficult and the diagnosis may eventually depend upon excluding other causes such as gout or septic arthritis.

56. Thank you

57. The serum urate concentration may reduce during an acute attack; a normal urate concentration at this point does not rule out a diagnosis of gout

58. “ Eunuchs do not take gout, nor become bald. A women does not take gout unless her menses be stopped,An young man does not take gout unless he indulges in coitus. In gouty affection, inflammation subsides in 40 days ” hippocrates