SOAP. – Osteoarthritis

Osteoarthritis

Jill C. Cash and Julie Barnes

Definition

A.Osteoarthritis (OA), formerly known as degenerative joint disease, is a painful, chronic noninflammatory disease that affects one or more movable joints. It is characterized by destruction of the cartilage with resultant decrease in the joint spaces and bony overgrowth. OA is considered to be primary when there are no underlying conditions, and secondary to conditions such as trauma, septic arthritis, inflammatory arthritis, metabolic disorders, or congenital or acquired joint abnormalities.

Incidence

A.It is estimated that up to 12% of the general population between the ages of 25 and 74 years have OA. The incidence clearly increases with age as up to 85% of the general population older than 65 years of age have radiographic changes suggestive of OA.

Pathogenesis

A.Damage to the articular cartilage and subchondral bone may be because of local trauma and results in chondrocyte injury.

B.Chondrocytes release proteolytic enzymes that assist in repair of the cartilage.

C.In OA, the remodeling process of chondrocytes and release of enzymes is impaired and results in a loss of strength and greater trauma and destruction of the subchondral bone. The end result is joint destruction and bony overgrowth, most frequently in hands, knees, hips and spine.

Predisposing Factors

A.Increasing age: Among patients older than 55 years.

B.Gender: Women are more commonly affected and exhibit greater disease severity.

C.Genetic predisposition; distal interphalangeal (DIP) joint involvement.

D.Trauma such as previous fractures, ligamentous injuries, or occupationally related repetitive stress.

E.Altered joint anatomy or instability.

F.Obesity: Mechanical injury in the knee may increase OA.

G.Secondary inflammation such as infections, inflammatory arthropathies, and metabolic disorders.

Common Complaints

A.Unilateral joint pain frequently involving the joints of the hands, neck, lower back, knees, and hips.

B.Morning stiffness lasting less than 1 hour.

Other Signs and Symptoms

A.Unilateral joint pain involving the DIP and proximal interphalangeal (PIP) joints, first carpometacarpal joint, hips, knees, cervical and lumbar spine, and first metatarsophalangeal joint.

B.Mild OA, or early disease, pain that increases with joint use and decreases with rest.

C.Severe OA, or late disease, pain that is present with rest.

Subjective Data

A.Elicit the patient’s age at onset of pain.

B.Has the pain gradually gotten worse over the months or years?

C.How long does the pain last in the morning? Does the pain get worse with joint use and better with rest?

D.What joints are involved?

E.Is the joint pain described as aching?

F.What does the patient take to relieve the pain?

G.Is there any joint deformity, redness, swelling, or warmth?

H.Is there any decrease in range of motion (ROM) of the joint?

I.Is there any family history of OA?

Physical Examination

A.Check pulse and blood pressure (BP).

B.Inspect the joints for enlargement, edema, and erythema.

C.Palpate:

1.Palpate the joints, noting temperature, edema, and tenderness. Joints are cool; bony enlargement may be present in the PIP (Bouchard’s nodes) or DIP joints (Heberden’s nodes) and other weight-bearing joints.

2.Palpate extremities. Perform assisted and active ROM exercises. With examination, limited ROM of the joint and/or pain on palpation may be present, along with crepitus.

Diagnostic Tests

A.Erythrocyte sedimentation rate (ESR): OA does not cause an increase of the ESR.

B.Chemistry profile.

C.Complete blood factor (CBC).

D.Rheumatoid factor (RF).

E.Routine radiography: Confirms disease severity and presence of joint narrowing.

F.CT scan or MRI: Considered with nerve impingement syndrome (spine) or spinal stenosis.

Differential Diagnoses

A.Inflammatory OA.

B.Rheumatoid arthritis (RA).

C.Gout or pseudogout.

D.Septic arthritis.

E.Bursitis or tendonitis.

F.Systemic lupus erythematosus (SLE).

G.Fracture or trauma.

Plan

A.General interventions:

1.Confirm diagnosis.

2.Provide the patient with support and education to improve patient well-being and reduce discomfort.

3.Physical therapy and/or occupational therapy should be initiated, if indicated.

B.Patient teaching:

1. See Section III:Patient Teaching Guide Osteoarthritis.

2.Reinforce the importance of joint protection; avoid repetitive stress or trauma.

3.Encourage daily exercises and strengthening, which improve strength, flexibility, and balance, reduce pain, and improve function.

4.Encourage weight loss if the patient is obese. Knee OA progression linked to obesity. Risk lowered with weight loss and level of joint pain may be significantly reduced.

C.Pharmaceutical therapy:

1.First-line agents: The goal of treatment is to preserve joint mobility. First-line agents should be used in a stepwise approach:

a.Acetaminophen up to 1 g four times daily; in early disease, this may be given on an as-needed basis.

b.Nonsteroidal anti-inflammatory drugs (NSAIDs) if acetaminophen has failed to control the pain. Use with caution. Consider renal function and risk factors for peptic ulcer disease (PUD) and cardiovascular disease (CVD).

i.Naproxen 220 to 375 mg one to two times daily.

ii.Inflammatory OA: Consider naproxen 375 to 500 mg twice a day. Recommend taking this medication for 2 to 4 weeks for maximum effects.

iii.Ibuprofen 200 to 400 mg, three times a day, may also be considered. Doses may be

increased at a gradual pace for maximum benefit as tolerated. If one NSAID does not work consider other NSAIDs.

•Cox-2 inhibitors, such as celecoxib (Celebrex), may also be considered. Celebrex 200 mg daily to twice a day as tolerated.

•Meloxicam (Mobic) 7.5 to 15 mg daily.

c.For high-risk patients, an H2 receptor blocker may decrease gastritis and be helpful in preventing duodenal ulcers. Consider Arthrotec 50: One tablet three times a day.

d.Misoprostol may be considered in patients who are at high risk of gastric ulcers. It should not be used by pregnant women. It is considered high risk for fetal death and possible congenital abnormalities.

e.Topical creams:

i.Diclofenac gel (Voltaren gel) may be applied to affected area; recommended for patients with severe pain who are not able to tolerate oral NSAIDs.

ii.Capsaicin cream may be applied to the affected area. Capsaicin creams may cause local burning at the site of application for the first several days.

2.Second-line agents: Second-line agents, such as intraarticular corticosteroid injections, may prevent some joint erosion and decrease pain. The same joint should not be injected more than three to four times a year in 3-month intervals. If the joint is injected at this frequency for more than 1 year, alternative options, such as surgery, should be considered. Narcotics may provide relief from more severe OA pain, but they carry a risk of dependence. Narcotics should be reserved for patients who do not respond to other treatments and are not surgical candidates. Follow state protocols for scheduled pain medications.

3.The use of glucosamine and chondroitin has not been established and is not recommended for patients. There does not appear to be any risks associated with using glucosamine and chondroitin. If the patient does not notice any relief within the first 6 months of use, then recommendations are to discontinue this product.

4.Physical therapy to create an individualized exercise regimen to strengthen muscles, increase ROM, and reduce pain

5.Lubrication injections (Hyalgan or Synvisc) may also be considered. Referral to the rheumatologist should be considered for this treatment.

Follow-Up

A.Follow-up is based on disease severity and therapeutic treatment. If the patient is treated with first-line agents, follow-up on pain control, nonpharmocological interventions, and possible side effects of medications within 2 to 4 weeks.

Consultation/Referral

A.Referral to an orthopedic surgeon may be considered for moderate to severe pain as indicated.

Individual Considerations

A.Pregnancy:

1.NSAIDs should not be used in pregnancy unless clearly indicated. Misoprostol should be used with great caution in women of childbearing age because of its potential for fetal abnormalities and abortive properties.

B.Adults and geriatrics:

1.Patients on chronic NSAIDs should be monitored closely for toxicity such as renal insufficiency, gastritis, and PUD. Elderly patients and those with preexisting GI disease, diabetes, congestive heart failure, and cirrhosis should be monitored closely.

2.Topical therapies are preferred for patients over age 75 due to increased risk for complications from oral NSAIDs.

3.Studies indicate that patients who adhered to the Mediterranean diet had a significantly lower prevalence of OA. The Mediterranean diet is high in beta carotene, omega 3, and magnesium, which research has suggested actively reduces inflammatory markers and OA-related pain. Some patients lose weight on the diet, which alleviates burden on the knees and decreases the inflammatory response.

4.Sedentary lifestyle contributes to OA disease and progressive pain. Studies have conjectured that pain coping skill training implemented to geriatric population improved self-efficacy for controlling OA-related knee pain, increasing physical functions and enhancing daily physical activities that improved quality of life.

5.Use with caution or avoid splinting/orthotics for long periods (≥6 weeks) secondary to geriatric patient’s vulnerability to periarticular muscle weakness and wasting. Splints worn at night may decrease pain and prevent unintentional injury with body positioning during sleep.