Ace the Case: A 55-Year-Old Woman With Bilateral Hand Pain

Clinical Review

Osteoarthritis is one of the most common causes of chronic disability in adults due to pain and altered joint function that can affect both single and multiple joints.2 The most commonly affected joints include knees, hips, interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints, as well as facet joints of the lower cervical and lumbar spine.2 Generalized OA of the hand typically involves multiple joints and progresses over time, with classic clinical findings of heberden (DIPs) and bouchard nodes (PIPs), as well as squaring of the first carpometacarpal.2 The physical examination of the patient above shows bony enlargement of DIPs and PIPs, suggestive of heberden and bouchard nodes, respectively. Osteoarthritis symptomatology includes joint pain, joint line tenderness, limitation in range of motion, bony swelling, joint deformity, and instability.3 Pain in OA is usually worse with joint use and is relieved with rest. Symptoms are generally worse in the late afternoon and early evening but can also be worse in the morning,3 as seen in the current patient.

Multiple risk factors have been linked to the pathogenesis of OA, including age, joint injury, obesity, genetics, gender, and anatomical factors, such as joint shape and alignment.4 The incidence of OA increases with age and is higher in women than men. The reason for its increased risk in women is unclear, although it is possibly related to hormones because estrogen is thought to protect cartilage from inflammation.

Pathophysiology

Inflammatory mediators may play a role in the pathogenesis of OA as potential contributors to joint tissue destruction. Several cytokines and chemokines have been found in synovial fluid or noted to be produced by articular chondrocytes, including IL-1, IL-7, IL-8, IL-17, IL-18, TNF-alpha, macrophage inflammatory protein-1 beta, and damage-associated molecular patterns.5,6 There is growing evidence that OA is associated with activation of the innate immune response, which can be initiated by tissue damage.5,7 These proinflammatory factors appear to be driving the production of the proteolytic enzymes responsible for the degradation of the extracellular matrix that results in joint tissue destruction.7

Diagnosis and Clinical Manifestations/Monitoring

Osteoarthritis can be diagnosed without the use of radiography or laboratory tests if there are typical signs and symptoms in an at-risk group (usage related to joint pain, age older than 45 years, morning stiffness less than or equal to 30 minutes). However, the most commonly used modality to diagnose OA is conventional radiography. Characteristic features on imaging include joint space narrowing, marginal osteophytes, subchondral sclerosis, and cysts.8 The prevalence of radiographic hand OA in the United States has been reported to range from 27% to more than 80%.8 There can be discordance between symptoms and radiographic disease because not all patients with radiographic disease experience symptoms and not all patient with symptoms have radiographic disease.9 The prevalence of symptomatic hand OA increases with age, with one study reporting 13% of men and 26% of women older than age 70 years reported symptomatic hand OA.9 Evaluation of synovial fluid is generally non-inflammatory or mildly inflammatory, with less than 2000 WBC/mm3. Typically, inflammatory fluid with greater than 2000 WBC/mm3 is associated with rheumatoid arthritis, psoriatic arthritis, inflammatory bowel disease associated arthritis, and microcrystalline arthritis.3

The most commonly used tools to assess pain in patients with hand OA are the Australian/Canadian Hand OA Index (AUSCAN) and the visual analog scale.10 The AUSCAN is a questionnaire containing 15 questions targeting areas of pain, stiffness, and physical function. Two separate studies were conducted: the first addressing the reliability and validity of AUSCAN and the second addressing AUSCAN index responsiveness.9 It was determined that the AUSCAN index is reliable, valid, and responsive and was recommended as the primary outcome measure for future hand OA clinical trials.10

The differential diagnosis for OA depends on the location of joint involvement and the presence or absence of additional systemic symptoms. The differential diagnosis includes rheumatoid arthritis, psoriatic arthritis, crystalline arthritis, hemochromatosis, infectious arthritis, and other soft-tissue abnormalities.

Treatment

The treatment goals for hand OA are to minimize pain, improve functionality, and slow the process of joint damage. The primary aim of clinicians should include targeting modifiable risk factors.11

Recently, the European League Against Rheumatism published updated guidelines for the management of hand OA. An international task force of 19 clinicians, healthcare professionals, and patients from 10 European countries developed 5 overarching principles in the management of hand OA:12

  1. Primary goals are to control symptoms, such as pain and stiffness, and to optimize hand function to maximize activity, participation, and quality of life.
  2. All patients should be offered information on the nature and course of the disease, as well as education on self-management principles and treatment options.
  3. Management of hand OA should be individualized, taking into account its localization and severity, as well as comorbidities.
  4. Management of hand OA should be based on a shared decision between the patient and the health professional.
  5. Optimal management of hand OA usually requires a multidisciplinary approach. In addition to nonpharmacological modalities, pharmacological options and surgery should be considered.

Nonpharmacologic interventions are the mainstay of OA management. Nonpharmacologic approaches include education (to enhance the patients understanding of their disease), self-management programs (targeted at behavioral modifications), and splints (particularly in patients with symptomatic OA at the base of the thumb). Splints for OA in the DIP joints are available but are less frequently used. One prospective cohort study with 25 patients demonstrated that splint treatment significantly reduced hand pain,13 although an open-controlled trial investigating DIP splints in 26 patients found no positive effects of nighttime DIP joint splinting on pain or function at 3 months follow-up.14 Exercise regimens can be implemented involving both range of motion and strengthening exercises. When nonpharmacologic therapies have been exhausted or are unlikely to be of significant benefit, pharmacologic agents can be used during periods when symptoms are present because no medication has been shown to be disease modifying. The main medications used in the management of hand OA include oral and topical nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and intra-articular glucocorticoids.15 Topical NSAIDs have not been studied as extensively in hand OA as they have been in patients with knee OA. A Cochrane review including 39 studies demonstrated that topical NSAIDs were effective in relieving pain in patients with chronic musculoskeletal complaints, mostly due to OA (number needed to treat: 10; 95% confidence interval: 7-16).16 When conservative and pharmacologic options do not provide adequate relief, surgical management may be an option. Surgical intervention is most often done in thumb-base OA, although arthroplasty and arthrodesis of the DIP and PIP joints are not uncommon in patients with severe hand OA. The use of glucosamine and chondroitin, as well as nutritional supplements, are not routinely recommended due to lack of strong supporting evidence.

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What is the most appropriate treatment to initiate for this patient?
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Correct Answer: C.

Rationale: Acetaminophen the most appropriate treatment to initiate for this patient. The treatment of hand OA includes nonpharmacologic approaches including education (to enhance the patients' understanding of their disease) and splints (particularly in patients with symptomatic OA at the base of the thumb). Splints for OA in the DIP joints are available but are less frequently used.14 Pharmacologic therapies include acetaminophen, oral or topical NSAIDs, topical capsaicin, intra-articular glucocorticoids, or duloxetine. There is a lack of clear beneficial evidence for nutritional supplements (ie, glucosamine, chondroitin, or fish oil). There is no indication for systemic corticosteroids in this patient. Her history of hypertension and gastrointestinal bleed makes oral NSAIDs not an ideal therapy.

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