Sunday, January 9, 2022

Osteoarthritis/Degenerative Joint Disease Case File

Posted By: Medical Group - 1/09/2022 Post Author : Medical Group Post Date : Sunday, January 9, 2022 Post Time : 1/09/2022
Osteoarthritis/Degenerative Joint Disease Case File
Eugene C. Toy, MD, Gabriel M. Aisenberg, MD

Case 31
A 56-year-old woman presents to the office complaining of gradually progressive, nonpainful enlargement of the terminal joint on her left hand over a 9-month period. She has some stiffness with typing, usually in the afternoons. She also reports pain in her right knee, which occasionally “locks up.” The right knee hurts more after long walks. On examination, her blood pressure is 130/85 mm Hg, heart rate is 80 beats per minute (bpm), height is 5’8”, and weight is 285 lb with a body mass index (BMI) of 43.3 kg/m2. Examination reveals only a nontender enlargement of her left distal interphalangeal (DIP) joint, and the right knee is noted to have crepitus and slightly decreased range of motion (ROM). Those joints were not red or swollen.

What is your next step?
 What is the most likely diagnosis?
 What is the best initial treatment?
 What are the most important risk factors for this condition?
 What is the most effective way to prevent this condition?


ANSWERS TO CASE 31:
Osteoarthritis/Degenerative Joint Disease

Summary: A 56-year-old woman presents with
  • Normal vital signs
  • Obesity
  • Joint pain in the left DIP and right knee that worsens with activity
  • Crepitus and slightly decreased ROM of the right knee
  • No synovitis on examination

Next step: Obtain erythrocyte sedimentation rate (ESR) and plain x-rays of the hand and knee.
Most likely diagnosis: Osteoarthritis (OA), because the patient is obese and has pain that worsens with activity.

Best initial treatment: Nonsteroidal anti-inflammatory drug (NSAID) or acetaminophen for pain management.

Risk factors: Obesity, repeated trauma.

Prevention: Weight loss, regular exercise.


ANALYSIS
Objectives
  1. Identify the major clinical characteristics of OA. (EPA 1, 2)
  2. Describe the management of OA. (EPA 4)
  3. Understand the major classes of medications used for OA. (EPA 4)
  4. Differentiate OA from inflammatory arthritis. (EPA 1, 2)

Considerations
This patient’s history and examination are characteristic of OA. Laboratory work, typically negative for inflammatory arthritis, and x-rays would support the diagnosis, mostly by making other diagnoses less likely. The most important features are the gradual onset, the lack of active synovitis, and the fact that her symptoms worsen with activity. If there were evidence of inflammation or joint effusion, then the best next step would be to aspirate the fluid from the joint and send it for various studies, including Gram stain and culture to assess for infection, crystal analysis to assess for gout or pseudogout, and cell count to assess for inflammation.


APPROACH TO:
Osteoarthritis

DEFINITIONS
BOUCHARD NODES: Bony enlargement of proximal interphalangeal (PIP) joints, often asymptomatic.

CREPITUS: A creaking or hook-and-loop (Velcro)–like sound made by a joint in motion, typically not painful.

HEBERDEN NODES: Bony enlargement of DIP joints, often asymptomatic.

SYNOVITIS: Inflammation of the joint space characterized by redness, swelling, and tenderness to touch.


CLINICAL APPROACH
Pathophysiology
OA is the most common joint disease in adults. It is uncommon before age 40 but highly prevalent after age 60. The disease affects women more often than men. OA begins insidiously, progresses slowly, and eventually may lead to disability, recurrent falls, inability to live independently, and significant morbidity.

It is critical to differentiate OA from other conditions that may present similarly since treatment is different. Periarticular pain that is not reproduced with passive motion suggests bursitis or tendonitis. Prolonged pain lasting for more than 1 hour after awakening points toward an inflammatory arthritis. Intense inflammation suggests one of the microcrystalline diseases (gout/pseudogout) or infectious arthritis. Systemic constitutional symptoms, such as weight loss, fatigue, fever, anorexia, and malaise, indicate an underlying inflammatory condition and generally demand aggressive evaluation; these underlying conditions include polymyalgia rheumatica, rheumatoid arthritis (RA), systemic lupus erythematosus, and malignancy.

Clinical Presentation
Patients with OA often experience joint stiffness, which occurs with activity or after inactivity (“gel phenomena”) and lasts for less than 15 to 30 minutes. This is in contrast to the morning stiffness of patients with an inflammatory arthritis, such as RA, which often lasts for 1 to 2 hours in the morning, upon wakening, and often requires warming, such as soaking in a hot tub, to improve. In early OA, there are no obvious findings. The knees and hips are the most commonly affected joints, followed by the hand and finger joints.

There may be some crepitus in the joint. Unlike in inflammatory arthritis, there is often no or minimal tissue swelling (except in the most advanced disease). Bony prominences, especially in the DIP/PIP joints, can occur later. Hard or bony swelling in the DIP joints are called Heberden nodes, whereas those affecting the PIP joints are called Bouchard nodes. Figure 31–1 shows a typical joint involvement in OA versus RA. Pain seen in OA typically can be reproduced with passive motion of the joint.

rheumatoid arthritis and osteoarthritis

Figure 31–1.
Joint involvement in rheumatoid arthritis (left) and osteoarthritis (right).



Labs/Imaging. Laboratory examination typically is unremarkable; inflammatory markers such as ESR, C-reactive protein, and white blood cells (WBCs) all are normal. Likewise, autoimmune studies such as antinuclear antibody (ANA), rheumatoid factor, and complement levels also are normal. If the joint is aspirated, examination of the synovial fluid also reflects a lack of inflammation: WBCs less than 2000/mm3, protein lower than 45 mg/dL, absence of crystals, and glucose equal to that in the serum. X-ray evaluation in OA may show osteophytes, which are the most specific finding of this disease. However, osteophytes may not be present in early stages of OA. Other characteristics seen on x-rays include joint space narrowing, subchondral sclerosis, and subchondral cysts.

Treatment
Education is critical. Encourage the patient to stay active because not using the joint can cause further immobility. Multiple short periods of rest throughout the day are better than one large period. In patients with OA who are overweight, weight loss of even modest degree may produce improvement in lower extremity joint pain and function. Other methods of unloading an osteoarthritic joint include canes and walkers, which can reduce joint forces at the hip by as much as 50% and are helpful in reducing the frequency of falls. Physical therapy in the form of heat applied to the affected joints in early disease is often helpful. Moist superficial heat can raise the threshold for pain, produce analgesia by acting on free nerve endings, and decrease muscle spasm.

Perhaps the most important intervention is having the patient maintain full/near-full ROM with regular exercise. Physical therapy and exercise improve functional outcome and pain in OA by improving flexibility and by strengthening muscles that support the affected joints.

Nonpharmacologic interventions should be tried first for pain management, for functional capacity, and for slowing the process of joint damage. Pharmacologic interventions should then be added for patients with inadequate symptom relief to further decrease the pain burden. The standard of care involves starting with oral or topical NSAIDs. NSAID use is contraindicated in patients with a history of peptic ulcers, cardiovascular disease (stroke, myocardial infarction), uncontrolled hypertension, kidney disease, or women in their third trimester of pregnancy due to premature closure of the patent ductus arteriosus. NSAIDs have a higher risk of gastrointestinal irritation and bleeding, and both NSAIDs and cyclooxygenase 2 (COX-2) inhibitors are associated with increased risk of adverse cardiovascular effects. Because of these risks, NSAIDs or COX-2 inhibitors should be used in the lowest dose necessary and for the shortest period in order to achieve symptom control. Nevertheless, NSAIDs are superior to acetaminophen in controlling pain among patients with OA.

Topical medications such as diclofenac, lidocaine, or capsaicin may be considered in patients who cannot tolerate oral NSAIDs or for those at higher risk for adverse effects (eg, patients over 75 years or those with significant cardiovascular disease). Duloxetine, a serotonin and norepinephrine reuptake inhibitor, has also been approved for knee OA.

The use of glucosamine and chondroitin for OA has been controversial, and results of randomized trials have varied. Though these medications appear to be safe, most studies suggest that glucosamine and chondroitin have little benefit in patients with OA.

Oral steroids are generally not used to treat OA. Intra-articular steroids are used for patients seeking short-term pain relief for moderate-to-severe pain flare-ups but are not useful for long-term treatment due to their relatively short duration of action (up to 6 weeks) and the possibility that long-term use may increase the rate of cartilage loss.

Surgery is reserved for only the most severe cases, which include patients who have major instability, a loose body in the joint (known as a joint mouse), intractable pain of advanced disease, or severe functional limitation. Arthroscopic debridement is widely used for those with symptomatic OA of the knee, especially with a meniscal tear, but clinical benefit is not supported by randomized clinical trials. Total joint arthroplasty (eg, knee replacement) is recommended for patients with severe symptomatic OA who fail to respond to optimal nonpharmacologic and medical therapy and for whom OA causes significant impairment in quality of life.


CASE CORRELATION
  • See also Case 32 (Low Back Pain), Case 33 (Acute Monoarticular Arthritis— Gout), and Case 34 (Rheumatoid Arthritis).

COMPREHENSION QUESTIONS

31.1 A 62-year-old woman presents to the office with severe knee pain that has been progressing over the past 5 years. The patient states that the current medications are ineffective. The provider has diagnosed the condition as advanced OA. Assuming that the diagnosis is correct, which of the following is most likely to be found in this patient?
A. Disability with recurrent falls and inability to live alone
B. Joints with redness and effusion
C. Best treated with oral steroids
D. Improvement throughout the day after approximately 1 to 2 hours of “unfreezing the joint”

31.2 A 72-year-old man with history of uncontrolled hypertension complains of painful joints in his hips and knees and the hands. Examination of the knees reveals pain with palpation and some crepitus upon movement, but no effusion or redness. The DIP and PIP joints are mainly affected in the hands; they similarly do not demonstrate effusion. Which of the following is the best initial treatment for this patient?
A. Naproxen sodium
B. Celecoxib
C. Oral prednisone
D. Intra-articular prednisone
E. Acetaminophen

Match the following disease processes (A-F) to the clinical setting described in Questions 31.3 to 31.6.
    A. Gonococcal arthritis
    B. Gout
    C. Pseudogout
    D. Osteoarthritis
    E. Rheumatoid arthritis
    F. Systemic lupus erythematosus

31.3 Symmetric bilateral ulnar deviation of both hands in a 42-year-old woman

31.4 Painful, swollen metatarsophalangeal great toe (unilateral) with redness and warmth after eating a steak and shrimp dinner in a 45-year-old man

31.5 Acute onset of unilateral elbow swelling, warmth, and tenderness and cervical discharge in a 25-year-old woman

31.6 Unilateral nontender bony enlargement of the first DIP and activity-related right hip pain in a 68-year-old woman


ANSWERS

31.1 A. This patient is presumed to have advanced OA. OA is a major cause of decreased functional status in elderly patients and requires ongoing treatment and evaluation by the clinician to try to improve symptoms and to promote mobility. Steroids are not a treatment of OA since it is not an inflammatory condition. Improvement with oral steroids (answer C) and activity throughout the day (answer D) are more characteristic of RA. Joints that exhibit redness and effusion (answer B) are more likely due to crystalline or septic arthritis.

31.2 E. Based on this patient having noninflamed joints and with the DIP and PIP joints of the hands affected, the most likely diagnosis is OA. RA would affect the knees and hips also, but usually with inflammation and effusion; in the hands, RA classically affects the metacarpophalangeal (MP) and PIP joints of the hands. Acetaminophen is the first agent of choice in the treatment of early OA. NSAIDs are superior in the treatment of OA; however, given this patient’s comorbidity of cardiovascular disease, NSAIDs (answers A and B) are relatively contraindicated. This is because of the association between NSAIDs and cardiovascular and renal disease. Thus, acetaminophen or topical NSAIDs would be better. Because this patient has a noninflammatory condition, neither oral nor intra-articular steroids are indicated (answers C and D).

31.3 E. Rheumatoid arthritis gives the ulnar deviation of the fingers by affecting the MP joints (in fact, one of the hallmarks of the disease). Other deformities associated with RA include the swan neck (MP flexion with PIP hyperextension and DIP flexion) and boutonniere (PIP flexion, DIP hyperextension) deformities.

31.4 B. Gouty arthritis often affects the first metatarsophalangeal joint of the feet and can be precipitated by alcohol or foods high in nucleic acids, like meats. There is often a familial predisposition. Uric acid crystals form in the joints and cause a severe inflammatory condition, redness, and pain.

31.5 A. Cervical discharge and inflammatory joint are consistent with gonococcal arthritis, which can also present as a migratory arthritis of large joints; this is an inflammatory condition with redness, pain, fever, and effusion.

31.6 D. The location and asymmetry of joint involvement, lack of inflammatory signs, and worsening with exertion all are characteristic of OA. RA is typically symmetric.


CLINICAL PEARLS

▶ Osteoarthritis is the most common articular disease of adults, most often affecting the DIP joints, PIP joints, knees, hip joints, and cervical and lumbar spine.

▶ The pathophysiology of OA is a “wear and tear” of the joint, leading to intra-articular cartilage erosion and decreased joint space on radiograph.

▶ Pain in OA is worsened with activity and is not associated with morning stiffness.

▶ Current pharmacologic agents do not modify or stop disease progression. Treatment is aimed at symptom relief.

▶ Initial pharmacologic therapy should be NSAIDs, unless a contraindication, such as cardiovascular disease, gastric ulcers, or chronic kidney disease, is present.

▶ Joint replacement for severe OA is reserved for patients with intractable pain despite medical therapy and for those with severe functional limitations.

REFERENCES

Felson DT. Osteoarthritis of the knee. N Engl J Med. 2006;354:841-848. 

Felson DT. Osteoarthritis. In: Jameson JL, Fauci AS, Kasper SL, et al, eds. Harrison’s Principles of Internal Medicine. 20th ed. New York, NY: McGraw Hill Education; 2018:2226-2232. 

Zhang W, Jones A, Doherty M. Does paracetamol (acetaminophen) reduce the pain of osteoarthritis? A meta-analysis of randomized controlled trials. Ann Rheum Dis. 2004;63:901-907.

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