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Osteoarthritis and HIV

for Health Care Providers

Osteoarthritis

Note: Some medications mentioned in this chapter may not be available on the VHA National Formulary. Consult VA pharmacists for alternatives.

Key Points

  • Osteoarthritis (OA) is a joint disorder caused by the progressive breakdown and eventual loss of cartilage of one or more joints.
  • Typical symptoms include joint pain exacerbated by activity and relieved by rest, morning stiffness, or stiffness after periods of inactivity.
  • Evaluation of OA includes plain X rays; distinction from other arthritides may include ESR and rheumatoid factor (RF) determinations and synovial fluid examination to rule out infection or crystal disease.
  • The goals of treatment are pain reduction, improvement of joint mobility, and prevention of functional impairment.
  • All patients should receive nonpharmacologic interventions, including weight loss counseling as indicated. Pharmacologic interventions should start with the lowest-risk intervention for the level of impairment (acetaminophen, NSAIDs, or injections) and proceed along the analgesic ladder and levels of intervention (opioids, arthroscopy, or other surgical procedures).

Background

OA is the most common form of arthritis in the United States. Risk factors include age, obesity, and history of joint trauma. Recreational running does not increase the risk of developing OA.

Veterans with HIV*

Osteoarthritis: 14%

*Veterans in the VA HIV Clinical Case Registry in care in 2007 who had an ICD-9 code corresponding to this condition

Definitions and Classification

  • OA (also called degenerative joint disease) is a disorder caused by the progressive breakdown and eventual loss of cartilage of ≥1 joints. OA usually affects weight-bearing joints.
  • OA can be idiopathic or secondary:
    • Idiopathic OA does not have a specific inciting cause, and typically involves the hands, feet, knees, hips, or spine.
    • Secondary OA is caused or enhanced by another condition such as trauma, calcium pyrophosphate dehydrate deposition disease (CPPD), or other bone or joint disorders such as osteonecrosis, rheumatoid arthritis, gout, septic arthritis, or Paget disease. This form of OA can present with atypical joint involvement.
  • Treatment of OA depends on whether it is noninflammatory or inflammatory. Symptoms of inflammatory OA include swelling, morning stiffness lasting >30 minutes, and night pain.

Diagnostic criteria for OA depend on the joint affected:
(Note that symptoms often wax and wane over time.)

  • Knee osteoarthritis = knee pain + ≥3 of the following:
    1. Age >50
    2. Morning stiffness for <30 minutes
    3. Crepitus on active motion of the knee (see Evaluation below)
    4. Bony tenderness
    5. Bony enlargement
    6. No palpable warmth
    • Other characteristics that add to the accuracy of the diagnosis: ESR <40 mm/hour, RF <1:40, synovial fluid with clear fluid and white blood cell (WBC) count of <2,000 cells/µL, and X rays showing osteophytes
    • Diagnostic criteria of knee pain + 5 of the 10 physical and laboratory features yield a sensitivity of 92% and specificity of 75% for OA; the addition of X-ray findings consistent with OA increases the specificity to 86%
  • Hand osteoarthritis = hand pain + ≥3 of the following:
    1. Bony enlargement of ≥2 of the following joints: 2nd or 3rd distal interphalangeal (DIP) joint or proximal interphalangeal (PIP) joint, 1st carpometacarpal (CMC, base of thumbs) of either hand
    2. Bony enlargement of ≥2 DIP joints
    3. Swelling of <3 metacarpophalangeal (MCP) joints
    4. Deformity of at least 1 of the joints listed in #1
    5. Hand OA is diagnosed clinically; diagnostic criteria (above): sensitivity 94%, specificity 87%; laboratory and radiology tests do not greatly impact diagnosis
  • Hip osteoarthritis = hip pain and ≥2 of the following:
    1. ESR <20 mm/hour
    2. Femoral or acetabular osteophytes on radiography
    3. Joint space narrowing on radiography
    • Diagnostic criteria (above): sensitivity 89%, specificity 91%
    • Other characteristics that add to the accuracy of the diagnosis: internal rotation of <15º, pain on internal rotation, morning stiffness, flexion <115º

Evaluation

Risk factors
  • Age >40 years
  • Obesity
HistoryAsk about history of:
  • Trauma
  • CPPD
  • Osteonecrosis
  • Rheumatoid arthritis
  • Gout
  • Septic arthritis
  • Paget disease
  • Reactive arthritis
Differential diagnosis
(Partial. Note that these may be superimposed on OA.)
  • CPPD: Typically affects knees, wrists, MCP joints, hips; check synovial fluid.
  • Gout: Typically affects great toes, ankles, knees, wrists; acute onset with intense swelling and pain; check synovial fluid.
  • Rheumatoid arthritis: MCP and PIP joint involvement typically prominent; stiffness is worse after resting the joint; check RF.
  • Infectious monoarticular disease: typically affects a single joint; check synovial fluid. Common organisms include Staphylococcus aureus, Streptococcus organisms, Neisseria gonorrhoeae, Borrelia burgdorferi. In immunocompromised patients, etiologies include gram-negative bacteria, mycobacteria, fungi, and mycoplasma.
  • Osteonecrosis or avascular necrosis (AVN): Typically involves the femoral or humeral heads; patients with HIV are at increased risk of AVN (4% of HIV-infected patients had AVN in one study). Patients typically present with pain, particularly with weight-bearing and motion. Groin pain is seen with femoral head involvement, shoulder pain with humeral head involvement. AVN has been associated with corticosteroids, testosterone, statins, weight training, alcohol consumption, tobacco smoking, and presence of anticardiolipin antibodies. Magnetic resonance imaging (MRI) is the most sensitive test for early diagnosis; plain X rays will show changes after months to 5 years from onset.
  • Bursitis: Frequently secondary to trauma; does not limit motion unless joint is involved. Most common sites include prepatellar, olecranon, trochanteric, and bursae. Consider bursal fluid aspiration to rule out infection.
Symptoms
  • Joint pain exacerbated by activity and relieved by rest
  • Morning stiffness or stiffness after periods of inactivity
  • Advanced disease: pain may be present with progressively less activity, eventually during rest and at night
  • Episodic flares: increases in pain and inflammation that may result from crystal disease
Physical examination
  • Examination with particular attention to joints:
    • Tenderness on palpation, usually without warmth or significant erythema
    • Effusions occasionally present
    • Crepitus: disruption of normally smooth surfaces of joints [Place hand on a joint, ask the patient to move that joint. If crepitus is present, bumps and cracks will be felt.]
    • Osteophytes: palpable bony enlargements along the joint periphery
  • Typical joints affected:
    • Hands: DIP and PIP with Heberden nodes (bony enlargements)
    • Feet: especially the great toe
    • Knees: osteophytes, effusions, crepitus, limited range of motion
    • Hips: pain and limited range of motion
    • Spine: C5, T8, L3; can lead to spondylosis (osteophytes from the vertebral body impinging on the spinal canal)
    • Shoulders: anterior shoulder pain at the glenohumeral joint
Imaging
  • Obtain plain X rays for patients with suspected OA
  • Radiographic changes in OA are insensitive in early disease and correlate poorly with symptoms; however, the following changes are fairly specific and make further imaging unnecessary:
    • Joint space narrowing
    • Osteophytes
    • Subchondral sclerosis
    • Subchondral cysts
  • Consider MRI of the knee in patients with knee locking, popping, or instability suggestive of meniscal or ligamentous damage (can be treated surgically).
  • Consider MRI if trying to rule out AVN
Diagnostic testing
  • Joint aspiration: When the patient has a joint with significant effusion or presence of warmth and erythema, obtain synovial fluid for examination (refer to Rheumatology or Orthopedic Surgery if needed). Request cell count, crystal analysis, Gram stain, and culture. In OA, the synovial fluid typically has mild pleocytosis, normal viscosity, and modestly elevated protein.
  • If the patient has sterile inflammatory synovial fluid (WBC >2,000 cells/µL and polymorphonuclear leukocytes [PMNs] >75% but no crystals and a negative culture), consider checking ESR (or C-reactive protein [CRP]), RF, and anti-cyclic citrullinated peptide (CCP) antibodies. Positive results can suggest a diagnosis of rheumatic disorder.
Diagnostic criteriaSee diagnostic criteria above for specific joints.

Management

  • The goals of treatment are pain reduction, improvement of joint mobility, and prevention of functional impairment.
  • All patients with OA should receive nonpharmacologic interventions in addition to analgesics, as indicated. Depending on noninflammatory vs inflammatory OA, advance up the analgesic and intervention "ladder":
    • acetaminophen or NSAIDs +/- adjuvants →
    • weak opioids +/- adjuvants →
    • strong opioids +/- adjuvants.
  • Obesity is the most important modifiable contributor to OA; all overweight patients should be encouraged to lose weight.
InterventionComments
Nonpharmacologic
  • Weight-loss programs as indicated
  • For acute flares, short periods of rest only (12-24 hours), followed by passive joint exercises
  • Range of motion and strengthening exercises that target weak muscle groups
  • Exercise programs involving exercises such as swimming, biking, walking, yoga, and tai chi
  • Knee OA: simple elastic sleeve brace or wedged shoe insoles to help reduce joint impact
  • Psychoeducation and cognitive-behavioral therapy (CBT) coping skills training
  • Acupuncture for peripheral joint OA has shown efficacy over sham acupuncture
  • Glucosamine and chondroitin alone or in combination do not appear to be more efficacious than placeb
Pharmacologic
(for dosages and additional information, see Pain Medications)
Capsaicin
  • Topical medication, for noninflammatory and inflammatory OA
Acetaminophen
  • First-line analgesia in noninflammatory mild OA
  • Possible adverse effects: hepatotoxicity (especially if taken with alcohol), nephrotoxicity (with chronic overdose)
  • Safer but less effective than NSAIDs for chronic OA
NSAIDs
(eg, ibuprofen, naproxen)
  • For persistent noninflammatory and inflammatory OA
  • Avoid in patients with peptic ulcer disease, renal disease, or cirrhosis
  • To minimize risks, use the lowest effective dosage (eg, <1,600 mg ibuprofen per day) and try to use for short periods of time
  • Avoid indomethacin: associated with increased joint destruction
  • COX-2 inhibitors (eg, celecoxib) have an increased risk of serious cardiovascular complications, and should be used only in patients with a history of or high risk of GI bleeding and no known CAD and absence of multiple CAD risk factors
Intraarticular corticosteroid injection
  • For moderate, persistent symptoms
  • Triamcinolone or methylprednisolone suspensions
    • Finger or toe joints: 10 mg
    • Wrists, elbows, ankles: 20 mg
    • Shoulder, knee, hip: 40 mg
  • Refer to rheumatologist or orthopedic surgeon if expertise is not available in clinic
  • Do not inject the joint if there is any suspicion of joint infection (clues include rapid onset of a large effusion, fever, leukocytosis)
  • Ensure aseptic technique
  • Possible adverse effects: tendon rupture (particularly with undiluted glucocorticoids in the shoulder), nerve atrophy if glucocorticoids enter the nerve sheath, skin changes, iatrogenic infection (rare)
  • Can repeat every 3 months for up to 2 years if effective
  • Hip injections are technically difficult and should be done under fluoroscopic guidance by a rheumatologist, orthopedist, or interventional radiologist
Colchicine
  • Consider for patients with refractory inflammatory OA: many have calcium pyrophosphate crystals in the synovial fluid
  • Use in conjunction with NSAIDs
  • Avoid use for patients with renal or hepatic disease
Opiate analgesics

Options include:
  • Use opioids for patients who have pain refractory to the interventions listed above (nonpharmacologic, capsaicin, acetaminophen, ibuprofen, injections, colchicine) or who cannot receive those interventions
  • Start with weak opioids and assess safety, efficacy, and usage; titrate up and move to stronger opioids as needed
Tramadol
(not a typical opiate; exact mechanism of action is unknown; acts in part as a central opioid agonist)
  • Use opioids cautiously with elderly patients
  • Opioid therapy for chronic pain should follow a fixed-dose schedule, not PRN dosing
  • Risk of dependence, overdose: monitor closely
  • Risk of constipation; give stool softener or laxative to prevent or treat constipation
  • Chronic opioid therapy should incorporate an opioid use agreement that includes functional goals for outcome, not reduced pain intensity alone
Weak opioids
  • Codeine
  • Hydrocodone + acetaminophen
  • Oxycodone + acetaminophen
  • Note that tramadol 37.5 mg + acetaminophen 325 mg has shown pain relief equivalent to codeine 30 mg + acetaminophen 325 mg but with fewer adverse effects (major adverse effect: headache): can provide additional pain relief when added to NSAIDs.
Strong opioids
  • Morphine
  • Oxycodone
  • Hydromorphone
  • Fentanyl transdermal
Surgical
Arthroscopic irrigation or debridement
  • For moderate persistent symptoms
  • Referral to an orthopedic surgeon
  • Irrigation with sterile saline
  • Suction of debris and blood
  • Removal of floating cartilage
  • Debridement of excess tissue or bone
  • Repair of tears as needed and to extent possible
Arthroscopic synovectomy
  • For inflammatory OA with profound impairment
  • Referral to an orthopedic surgeon
  • Arthroscopic removal of involved synovial tissue
Major surgical procedure
  • For end-stage OA, profound impairment
  • Referral to an orthopedic surgeon
  • Includes total joint replacement

References