Case study joint syndome osteoarthritis mj

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Case study joint syndome osteoarthritis mj

  1. 1. JOINT SYNDROMEOsteoarthritisRheumatoid ArthritisSLEGout
  2. 2. Osteoarthritis Osteoarthritis is a non-inflammatory, degenerative condition of joints Characterized by degeneration of articular cartilage and formation of new bone i.e. osteophytes.
  3. 3.  Common in weight-bearing joints such as hip and knee. Also seen in spine and hands. Both male and females are affected. But more common in older women i.e. above 50 yrs,particularly in postmenopausal age.
  4. 4. Risk factors Obesity esp OA knee Abnormal mechanical loading eg.meniscectomy, instability Inherited type II collagen defects in premature polyarticular O Inheritance in nodal OA Occupation eg farmers Infection:Non-gonococcal septic arthritisHereditaryPoor postureInjured joints
  5. 5. Ageing process in joint cartilageDefective lubricating mechanismIncompletely treated congenitaldislocation of hip
  6. 6. Classification of Osteoarthritis1- Localized –Ankle / knee/ hip/ spine/hands2- Generalized3- Erosive4- Crystal associated OAAccording to Nodules1- Nodular (Haberden’s, Bouchard’s)2- Non-Nodular
  7. 7. X-Ray Classification of OA1- No Osteophytes / Minimal changes2- Single osteophytes / Subchondrial sclerosis / Widening3- Significant narrowing, Multiple osteophytes4- Narrowing osteophytes, Deformity, Ankylosis
  8. 8. According to Limitation of Activity1- Patient is able to do physical activity2- Moderate decrease of physical activity3- Significant decrease of physical activity4- Total Ankylosis and no activity
  9. 9. Clinical features of OA Pain Stiffness Muscle spasm Restricted movement Deformity Muscle weakness or wasting Joint enlargement and instability Crepitus• Joint Effusion
  10. 10. Pain syndrome•Morning stiffness <20 mins•Pain is worst at the end of the day•Present muscular spasms•Inflammatory sinovits
  11. 11.  Movement abnormalities  ‘Gelling’: stiffness after periods of inactivity, passes over within minutes (approx 15min.) of using joint again  Coarse crepitus: palpate/hear (due to flaked cartilage & eburnated bone ends)
  12. 12. Deformities  Soft tissue swelling: ○mild synovitis ○small effusions  Osteophytes  Joint laxity  Asymmetrical joint destruction leading to angulation
  13. 13. Osteoarthritis of the DIPjoints. This patient hasthe typical clinicalfindings of advancedOA of the DIP joints,including large firmswellings (Heberden’snodes), some of whichare tender and red dueto associatedinflammation of theperiarticular tissues aswell as the joint.
  14. 14. Knee joint effusion
  15. 15. Special Investigations Blood tests: Normal Radiological features:  Cartilage loss  Subchondral sclerosis  Cysts  Osteophytes
  16. 16. COMPLAINS a. Patient complains of pain of insidious onset in the knee joints. The pain is aching and poorly localized. b. Pain first occurs after normal joint use and can be relieved by rest. As the disease progresses, pain during rest develops. Morning stiffness lasts less than a half hour. c. Systemic symptoms are absent.
  17. 17. varus angulationof the knee joints
  18. 18. Hallux valgus deformation
  19. 19. Varus angulationof the knee joints
  20. 20. RESULTS OF ANALYSES CBA- without pathology CUA- without pathology CRP 3 mg/l Synovial fluid is noninflammatory with less than 2000 white blood cells/mm3
  21. 21. OA-Plus tissue diseas(osteophytes)
  22. 22. X-ray of painful kneejoint
  23. 23.  PLAN OF TREATMENT?
  24. 24. TREATMENTA. Correction of predisposing factorsB. Patient educationC. Joint rest 1. Obesity. Weight reduction is important. 2. Malalignment. Valgus-varus knee deformity and eversion-inversion ankle deformity may require surgical correction. 3. Occupational changes may be necessary to protect diseased joints.D. Physical therapy 1. Therapeutic exercise. 2. Heat generally relieves pain and muscle spasm.E. Occupational therapy
  25. 25. Drug therapy• Analgesics Acetaminophen1. Nonsteroidal anti-inflammatory drugs Choice of NSAID.  Salicylates. - Enteric-coated aspirin. - Salsalate  Indoleacetic acid.  Oxicam.  Propionic acid.  Fenamic acid.  Pyrazolone.
  26. 26. NIMESULIDE
  27. 27. Less than 3 days. For sharp painLORNOXICAM
  28. 28. PATHOGENETICAL THERAPYChondroprotection a) systemic - 1500mg atleast 1yr, glucosamine, chondroitin sulfate, (most slowly influencing drugs b) local- Intrarticular injections (Hyaluronic acid, ) ), Traumeel, Alflutop) (A joint should not be injected more than 3 times a year. Intraarticular corticosteroids have an adverse effect on local car-tilage metabolism. )
  29. 29. Surgery 1. Indications a. Relief of pain or severedisability after failure ofconservative measures to reverseor alleviate the pathologic process. b. Correction of mechanicalderangement that may lead to OA.
  30. 30. Contraindications a. Infection. b. Poor vascular supply. c. Emotional instability or occupational factors that make surgical rehabilitation unlikely to succeed. d. Obesity (relative contraindication). e. Serious medical illness (relative contraindication).Knee procedures a. Osteotomy. b. Arthrodesis. c. Total knee prosthesis. d. Arthroscopic debridement.
  31. 31. Hip a. Osteotomy. b. Excision arthroplasty. . c. Arthrodesis. d. Total hip replacement
  32. 32. Joint replacement surgery (arthroplasty)
  33. 33. THANK YOU Manj -2012 KSMU

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