1 / 48

Approach to the patient with Monoarthritis

Approach to the patient with Monoarthritis. Diseases that commonly present with 1 joint:. Approach to the pt w/ Monoarticular sx: Diseases that commonly p/w monoarthritis. Septic: bacterial, mycobacterial, lyme, fungal Traumatic: fx, internal derangemt, hemarthrosis (sickle)

powa
Download Presentation

Approach to the patient with Monoarthritis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Approach to the patient with Monoarthritis • Diseases that commonly present with 1 joint:

  2. Approach to the pt w/ Monoarticular sx:Diseases that commonly p/w monoarthritis • Septic: bacterial, mycobacterial, lyme, fungal • Traumatic: fx, internal derangemt, hemarthrosis (sickle) • Crystal deposition: gout, CPPD, hydroxyapatite deposition disease, calcium oxalate • Other: OA, JA, coagulopathy, AVN bone, foreign-body synovitis, tumor

  3. Polyarticular diseases occasionally p/w one joint of onset • RA • JA • Viral • Sarcoid • ReA • PsA • IBD-arthritis • Whipples • OA

  4. Important questions? • What should you ask the patient? • What’s critical to determine ASAP? • What’s the most useful test to determine etiology? • What other labs/studies should be obtained?

  5. The patient with polyarticular symptoms • Diseases that present with acute polyarticular sx: • Chronic polyarticular sx?

  6. Acute polyarticular • Infection: GC, Meningococcal, lyme, ARF, BE, viral (hepatitis B/C, parvovirus, EBV, HIV) • Other inflammatory: RA, systemic JA, SLE, ReA, PsA, polyarticular gout, sarcoid

  7. Chronic polyarticular

  8. Chronic Polyarthritis • Inflammatory: RA, JA, SLE, SSc, polymyositis, ReA, PsA, gout, IBD, CPPD, sarcoid, vasculitis, PMR • Non-inflammatory: OA, FM, hypermobility syndrome, hemochromatosis • Migratory, Additive, Intermittent

  9. Evaluation and Management of Osteoarthritis

  10. Osteoarthritis: Case 1 • A 65-year-old man comes to your office complaining of knee pain that began insidiously about a year ago. He has no other rheumatic symptoms • What further questions should you ask? • What are the pertinent physical findings? • Which diagnostic studies are appropriate?

  11. Pain is related to use Pain gets worse during the day Minimal morning stiffness (<20 min) and after inactivity (gelling) Range of motion decreases Joint instability Bony enlargement Restricted movement Crepitus Variable swelling and/or instability OA: Symptoms and Signs

  12. OA Case 1: Radiographic Features • Joint space narrowing • Marginal osteophytes • Subchondral cysts • Bony sclerosis • Malalignment • MAKE THE DIAGNOSIS

  13. OA: Laboratory Tests • No specific tests • No associated laboratory abnormalities; eg, sedimentation rate • Investigational: Cartilage degradation products in serum and joint fluid

  14. Understanding Disease Mechanisms • OA is mechanically driven, but chemically mediated…

  15. Immunostain of OA Cartilage Melchiorri, et. al. 1998

  16. Spontaneous Production of Inflammatory Mediators by Normal and OA-affected Cartilage IL-18 PGE2 NO MCP-1 ELISA IL-8 IL-6 IL-1b TNFa 0 20 40 60 80 100 Units Attur et al. Osteoarthritis and Cartilage 2002

  17. Candidate Biomarkers in OA • CRP (obesity??) • COMP, Keratan sulfate, HA, YPL-70 • Type II collagen fragments • Type II C-propeptide (synthesis) • Proteoglycan/aggrecan fragments • Markers of bone turnover (osteocalcin,NTx) • Imaging (x-ray, MRI, ultrasound)

  18. OA: Risk Factors • Why did this patient develop osteoarthritis?

  19. OA: Risk Factors (cont’d) • Age: 75% of persons over age 70 have OA • Female sex • Obesity • Hereditary • Trauma • Neuromuscular dysfunction • Metabolic disorders

  20. Case 1: Cause of Knee OA • On further questioning, patient recalls fairly serious knee injury during sport event many years ago • Therefore, posttraumatic OA is most likely diagnosis

  21. Case 1: Prognosis • Natural history of OA: Progressive cartilage loss, subchondral thickening, marginal osteophytes

  22. OA: Case 2 • A 75-year-old woman presents to your office with complaints of pain and stiffness in both knees, hips, and thumbs. She also has occasional back pain • Family history reveals that her mother had similar problems • On exam she has bony enlargement of both knees, restricted ROM of both hips, squaring at base of both thumbs, and multiple Heberden’s and Bouchard’s nodes

  23. Distribution of Primary OA • Primary OA typically involves variable number of joints in characteristic locations, as shown • Exceptions may occur, but should trigger consideration of secondary causes of OA

  24. Age-Related Prevalence of OA: Changes on X-Ray Men Women DIP DIP Knee Prevalence of OA (%) Prevalence of OA (%) Knee Hip Hip Age (years) Age (years)

  25. Case 2: Distal and Proximal Interphalangeal Joints

  26. Case 2: Carpometacarpal Joint • Radiograph shows severe changes • Most common location in hand • May cause significant loss of function

  27. Case 2: Hip Joint • X-ray shows osteophytes, subchondral sclerosis, and complete loss of joint space • Patients often present with deep groin pain that radiates into the medial thigh

  28. What If Case 2 Had OA in the “Wrong” Joint, eg, the Ankle? • Then you must consider secondary causes of OA • Ask about previous trauma and/or overuse • Consider neuromuscular disease, especially diabetic or other neuropathies • Consider metabolic disorders, especially CPPD (calcium pyrophosphate deposition disease—aka pseudogout)

  29. Secondary OA: Diabetic Neuropathy • MTPs 2 to 5 involved in addition to the 1st bilaterally • Destructive changes on x-ray far in excess of those seen in primary OA • Midfoot involvement also common

  30. Hemochromatosis Hyperparathyroidism Hypothyroidism Hypophosphatasia Hypomagnesemia Neuropathic joints Trauma Aging, hereditary Underlying Disease Associations of OA and CPPD Disease (pseudogout)

  31. Management of OA • Establish the diagnosis of OA on the basis of history and physical and x-ray examinations • Decrease pain to increase function • Prescribe progressive exercise to • Increase function • Increase endurance and strength • Reduce fall risk • Patient education: Self-Help Course • Weight loss • Heat/cold modalities

  32. Pharmacologic Management of OA • Nonopioid analgesics • Topical agents • Intra-articular agents • Opioid analgesics • NSAIDs • Unconventional therapies

  33. Strengthening Exercise for OA • Decreases pain and increases function • Physical training rather than passive therapy • General program for muscle strengthening • Warm-up with ROM stretching • Step 1: Lift the body part against gravity, begin with 6 to 10 repetitions • Step 2: Progressively increase resistance with free weights or elastic bands • Cool-down with ROM stretching Rogind, et al. Arch Phys Med Rehabil. 1998;79:1421–1427. Jette, et al. Am J Public Health. 1999;89:66–72.

  34. Reconditioning Exercise Program for OA • Low-impact, continuous movement exercise for 15 to 30 minutes 3 times per week • Fitness walking: Increases endurance, gait speed, balance, and safety • Aquatics exercise programs—group support • Exercycle with minimal or no tension • Treadmill with minimal or no elevation

  35. Nonopioid Analgesic Therapy • First-line—Acetaminophen • Pain relief comparable to NSAIDs, less toxicity • Beware of toxicity from use of multiple acetaminophen-containing products • Maximum safe dose = 4 grams/day

  36. Nonopioid Analgesic Therapy (cont’d) • NSAIDs • Use generic NSAIDs first • If no response to one may respond to another • Lower doses may be effective • Do not retard disease progression • Gastroprotection increases expense • Side effects: GI, renal, worsening CHF, edema • Antiplatelet effects may be hazardous

  37. Nonopioid Analgesics in OA • Cyclooxygenase-2 (COX-2) inhibitors • Pain relief equivalent to older NSAIDs • Probably less GI toxicity • No effect on platelet aggregation or bleeding time • Side effects: Renal, edema • Older populations with multiple medical problems not tested • Cost similar to generic NSAIDs plus proton pump inhibitor or misoprostol Medical Letter. 1999;41:11–12.

  38. Nonopioid Analgesics in OA (cont’d) • Tramadol • Affects opioid and serotonin pathways • Nonulcerogenic • May be added to NSAIDs, acetaminophen • Side effects: Nausea, vomiting, lowered seizure threshold, rash, constipation, drowsiness, dizziness Medical Letter. 1999;41:11–12.

  39. Opioid Analgesics for OA • Codeine, oxycodone • Anticipate and prevent constipation • Long-acting oxycodone may have fewer CNS side effects • Propoxyphene • Morphine and fentanyl patches for severe pain interfering with daily activity and sleep

  40. Topical Agents for Analgesia in OA • Local cold or heat: Hot packs, hydrotherapy • Capsaicin-containing topicals • Use moderately supported by evidence • Use daily for up to 2 weeks before benefit • Compliance poor without full instruction • Avoid contact with eyes

  41. Intra-articular steroids Good pain relief Most often used in knees, up to q 3 mo With frequent injections, risk infection, worsening diabetes, or CHF Joint lavage Significant symptomatic benefit demonstrated Hyaluronate injections* Symptomatic relief Improved function Expensive Require series of injections No evidence of long- term benefit Limited to knees OA: Intra-articular Therapy * Altman, et al. J Rheumatol. 1998;25:2203.

  42. OA: Unconventional Therapies • Polysulfated glycosaminoglycans—nutriceuticals • Glucosamine +/- chondroitin sulfate: Symptomatic benefit, no known side effects • Doxycycline as protease/cytokine inhibitors • Under study • Have disease-modifying potential

  43. OA: Unconventional Therapies (cont’d) • Keep in touch with current information. • ACR Website (http://www.rheumatology.org) • Arthritis Foundation Website (www.arthritis.org)

  44. Referral and Imaging • If pain out of proportion to XRAY findings, can refer to rheum or ortho, and get MRI • Also, for unstable joints, need MR • Primary or secondary failure of treatment regimen should prompt further imaging and referral • Please obtain imaging BEFORE THE PATIENT GETS TO THE CONSULTANT • If there is any question of systemic inflammatory disease, check labs including CBC, ESR, CRP, rheumatoid factor, anti-CCP, (ANA), IgGs as well

  45. Surgical Therapy for OA • Arthroscopy • May reveal unsuspected focal abnormalities • Results in tidal lavage • Expensive, complications possible • Osteotomy: May delay need for TKR for 2 to 3 years • Total joint replacement: When pain severe and function significantly limited

  46. OA: Management Summary • First: Be sure the pain is joint related (not a tendonitis or bursitis adjacent to joint) • Initial treatment • Muscle strengthening exercises and reconditioning walking program • Weight loss • Acetaminophen first • Local heat/cold and topical agents

  47. OA: Management Summary (cont’d) • Second-line approach • NSAIDs if acetaminophen fails • Intra-articular agents or lavage • Opioids • Third-line • Arthroscopy • Osteotomy • Total joint replacement

More Related