Clinical presentation of osteoarthritis (OA)

  • Various degrees of inflammation but NO systemic effects
  • Mainly affects weight bearing joints (causes pain, limits range of motion, disability & QOL)
  • Incidence & severity increase with age (more commonly affects women)
  • Primary osteoarthritis (idiopathic) is the most common type
  • Localized = 1-2 sites
  • Generalized = 3+ sites
  • Erosive = erosion & proliferation of PIP & DIP joints
  • Hypertrophic phase (early):  cartilage swelling is present but usually asymptomatic with normal radiograph
  • Degradation of cartilage (eventual):  joint space narrowing & erosion of cartilage results in brittle, stiffer bone.  Characterized by inflammatory changes & pain which lead to decreased function & motion
  • S/S:  pain in affected joints (hands, knees, hips are most common), pain with motion, joint stiffness at rest, crepitus, limited ROM, joint enlargement, joint deformity, abnormal radiograph

Risk factors for the development of OA

  • Age, obesity, previous occupation or some sports, history of joint trauma, genetic predisposition

Nonpharmacologic interventions for OA

  • Treatment may relieve pain or improve function but it doesn’t reverse preexisting damage to cartilage
  • Education about the disease process, the extent of OA, prognosis & treatment options
  • Diet & exercise:  excess weight increases load on weight-bearing joints, weight loss will decrease symptoms & disability, need to motivate the patient with a structured weight loss program
  • PT & OT:  hot & cold treatments, quadricep strengthening, walking (depends on the pt, some will get worse), orthotic devices (canes, etc)
  • Surgery:  for functional disability & pts with unresponsive severe pain

Treatment options for OA:

  • acetaminophen, NSAIDs/COX-2 inhibitors, topical therapies, intra-articular steroid injections, hyaluronate injections, opioid analgesics, and glucosamine and chondroitin
  • APAP:  first line therapy for pain
    • Safe, effective, low cost analgesic & antipyretic that inhibbits the synthesis of PGs in the CNS by block the action of COX
    • 325-650 mg q 4-6  h
    • SE:  liver & kidney toxicity, risk of GI bleed in chronic alcohol users
    • DDI:  high doses can prolong warfarin’s half life, food decreases APAP concentration but not efficacy, other hepatotoxic drugs
  • NSAIDs:  second line therapy for pain
    • Antiinflammatory (at high doses), analgesic & antipyretic that blocks PG synthesis through the inhibition of COX
      • NSAIDs inhibit COX-1 & COX-2 enzymes
        • COX-1 is responsible for producing prostaglandin mediated gastroprotection, platelet aggregation, renal function
        • COX-2 is inducible with inflammation.  This enzyme is responsible for producing prostaglandins that mediate pain, fever, renal function
    • SE:  GI, CV, renal, prolonged bleeding time, increases BP, CNS effects, avoid ASA in kids (Reye’s syndrome), hepatitis
      • GI:  NSAIDs inhibit gastroprotective PG synthesis, minor complaints are common.  Potential GI SE:  GI bleed, peptic ulcer, GI perforation, abdominal pain, dyspepsia, flatulence, diarrhea, anorexia
        • Risk factors for GI toxicity:  > 65, comorbidities, use of oral glucocorticoids, history of PUD, history of GI bleed, using anticoags,
        • How to decrease risk:  use a COX-2 or NSAID + PPI or NSAID + misoprostol
      • CV:  biggest problem is associated with COX-2 inhibitors, traditional NSAIDs don’t show a significant increase in risk
        • To decrease risk of GI & CV SE give the COX-2 inhibitor with a PPI
      • Renal:  NSAIDs cause direct toxicity & inhibition of PGs that promote renal vasodilation
        • Lab values:  increase SCr, BUN, K
          • Monitoring:  SCr, CBC, BP, LFTs, edema
        • Risk factors:  HF, severe hepatic disease, chronic renal failure, nephrotic syndrome, elderly
          • Drugs:  diuretics, ACE-I, cyclosporine, aminoglycosides
        • Use APAP to avoid renal SE
    • DDIs with NSAIDs:  warfarin, antihypertensives, ACE-I, cyclosporine, methotrexate, digoxin, Li, IBU + cardioprotective ASA
    • DDIs w/ celebrex:  sulfa drugs, antidepressants, fluconazole, rifampin, carbamazepine, phenytoin
  • Topical therapies:
    • May be used as either adjuvant or monotherapy
    • Capsaicin depletes substance P from the nerve fibers & is available in 0.025-0.75% strengths OTC
      • Need to apply 2-4 times a day & it may take up to 2 weeks to work
      • Causes a temporary burning sensation so it’s important to wash hands after application
    • Diclofenac locally inhibits COX-2 enzymes
      • Topical formulation minimizes systemic exposure & the risk of serious SE
      • Apply to affected area 4 times daily
  • Glucosamine & chondroitin stimuate proteoglycan synthesis from articular cartilage
    • Glucosamine = 1500 mg/day              chondroitin = 1200 mg/day
    • Excellent safety profile but contraindication with shellfish allergy
  • Corticosteroids
    • Don’t use systemic steroids use intra-articular (injections into the joint)
    • Triamcinolone hexacetonide or methylprednisolone acetate
      • May have local & systemic SE
        • Limited to 3-4 injections per year to avoid systemic effects
      • Initial relief lasts 24-72 hours, peaks in 1 week & lasts up to 4-8 weeks
  • Hyaluronate injections
    • Intra-articular hyaluronic acid provides lubrication with motion, shock absorbency & some anti-inflammatory effects
    • Give once weekly for 3-5 weeks
    • May beneficial in unresponsive patients (we tolerated, minimal SE, expensive)
  • Opioid analgesics
    • Low-dose, sustained release formulations are recommended when other therapy options have been exhausted
    • Consider joint replacement over chronic opioid use
    • Tramadol:  modest analgesic effects in osteoarthritis, opioid-like SE

Step-wise approach to osteoarthritis treatment

  • Nonpharmacological therapy:  education, exercise, weight control, physical therapy, occupational therapy, assistive devices
  • Pharmacological therapy:  APAP, NSAIDs, COX-2 inhibitors, adjunctive analgesics, topical agents, nutritional supplements
  • Intra- articular injections:  hyaluronic acids, corticosteroids
  • Opioid analgesics
  • surgery

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