Epidemiology

An estimated 20 million people in the United States have osteoarthritis (OA), and 2 to 3 million have rheumatoid arthritis (RA). The total cost of medical care, lost work time, and disability for OA alone is estimated to run 2% of the gross national product. The most common cause of joint pain is OA, but the most crucial challenge is identification of a septic joint. Septic arthritis occurs in all age groups but is more common in children than in adults, and about 10% of patients with an acutely painful joint will be found to have infection.¹

Pathophysiology

The structure of diarthrodial joints (the most common type) includes the synovium, synovial fluid, articular cartilage, intraarticular ligaments, joint capsule, and juxtaarticular subchondral bone. The delicate synovium provides oxygen and nutrients to cartilage and produces lubricants. Articular cartilage deforms under mechanical load to minimize stress and provides a smooth surface for joint motion with minimal friction. Causes of joint disorders (Box 107.1) often overlap. Cumulative microdamage and remodeling occur with use and aging. Mechanical or metabolic disturbances may lead to a secondary inflammatory response, or an inflamed structure (e.g., a tendon) may rupture. Arthrosis is due to a mechanical insult, whereas arthritis is due to inflammation of the synovium. With inflammation comes white blood cell (WBC) infiltration, release of cytokines (e.g., tumor necrosis factor-α [TNF-α], interleukins) and other inflammatory mediators, and proliferation of cells or tissue. Edema collects around the joint, which causes stiffness. With prolonged inflammation, erosion of bone and destruction of the joint eventually occur and can produce deformity and chronic disability.

In addition to bone, muscles, and joints, “joint” pain may derive from nerves, skin, or periarticular structures (ligaments, tendons, bursae, bone). The enthesis is the structural insertion of tendon or ligament into bone. Inflammatory enthesitis is prominent in the spondyloarthropathies, such as reactive arthritis.

Presenting Signs and Symptoms

The clinical findings can narrow the potential cause of a patient’s symptoms (Table 107.1). Initial assessment must determine whether the anatomic site of the problem is the joint and then a general category of the disease, either inflammatory (septic versus aseptic) or noninflammatory (mechanical). A red, hot, swollen, painful joint is the classic finding with septic and other inflammatory arthritides. Arthritis patients may also have serious nonarticular complications of their disease or its treatment.

The onset and pattern of pain are important to determine (Box 107.2). Mechanical pain is worse with use, rapidly relieved with rest, and often least in the morning. If present, morning stiffness resolves quickly. Rapid onset over a period of minutes suggests trauma, internal derangement, or a loose fragment in the joint. Inflammatory pain is often worse with use as well, but not so quickly relieved with rest, and is commonly associated with morning stiffness (short duration with OA, prolonged with RA). “Gelling” (stiffness and immobility) after sitting in one position occurs with either type. Widespread pain with stiffness is typically due to inflammatory arthritis or fibromyalgia. Subjective pain without joint findings on examination is termed arthralgia. If the patient has tried medications without relief, the dosage should be determined because inadequate dosing is common.

Although pain is usually the main concern of patients with joint disease, it is important to determine whether other associated symptoms (e.g., fever, rash, eye symptoms) or findings are present that can aid in the diagnosis. For example, examination of the skin may reveal the malar or butterfly facial rash associated with lupus, the pustular lesions of gonococcemia, or the subcutaneous nodules of RA and gout.

The musculoskeletal examination attempts to identify the exact site of the problem—joint versus bone, muscle, periarticular, or superficial skin pain. Particular joint involvement may aid in making the diagnosis (Box 107.3). True joint pain is usually diffuse on palpation and increases with active and passive motion. Periarticular inflammation (tendonitis, bursitis, cellulitis) is generally more focal, with pain reproduced only by certain movements—most often resisted active contraction or passive stretching of the involved muscles or tendons and usually only toward one side.

Differential Diagnosis and Medical Decision Making

Mechanical, inflammatory, or metabolic causes of arthritis may be present, and the whole picture must be considered in narrowing the lengthy differential diagnosis (Box 107.4). A new diagnosis of a specific type of inflammatory arthritis may not be possible in one visit, but recognition that the case is inflammatory is important for interim care. The severity of a patient’s discomfort will determine the urgency of analgesia, which may be initiated well before refining the list of possible diagnoses.

Early identification of septic arthritis is a top priority. An infected joint is especially likely to be present in patients with inflammatory, acute monarticular arthritis, with or without fever. The presence of another site of infection (skin, lungs, urine, heart) or a joint prosthesis increases the likelihood considerably. Moderate fever is typical with a septic joint, whereas low-grade fever may be present with any inflammatory arthritis. Treatment (antibiotics and drainage) must be initiated empirically while awaiting culture results. Infections in nearby sites (bursae, skin, periosteum) should be distinguishable by careful examination and radiologic studies; ultrasonography may be very helpful in looking for joint effusions. High fever, chills, and signs of sepsis should prompt fluid resuscitation as needed and studies to identify any additional site of infection.

Although patients usually have a history of trauma or very sudden monarticular pain, fractures may occasionally be surprises, especially in those with severe osteopenia or altered mentation (e.g., alcohol abuse, seizures), in whom trauma might not have been noticed.

Signs and symptoms may overlap, but crystals found on arthrocentesis are diagnostic of crystal-induced arthritis. The recent addition of a medication that can cause hyperuricemia may be a clue, but serum uric acid levels alone do not make or rule out the diagnosis of gout. Frequently, the patient has had multiple bouts of gout in the same joint, most commonly the great toe.

Diagnostic Studies

Blood tests are rarely diagnostic in patients with synovial disorders but may be ordered sparingly to assist in management decisions. A complete blood count (CBC) and basic chemistry profile will identify anemia, an elevated WBC count, and renal dysfunction (which affects selection of medications). The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are nonspecific but useful markers of inflammation. Coagulation studies are needed only if a patient is taking anticoagulants or a bleeding disorder is suspected. Creatine phosphokinase is helpful if muscle pain or weakness is detected. If clinical assessment raises concern for other autoimmune or systemic diseases, additional screening for multiorgan involvement with urinalysis, liver enzymes, electrocardiogram, and chest films may help. Serologic testing (e.g., rheumatoid factor [RF], antinuclear antibody, and Lyme serology, depending on the clinical impression) is generally done in follow-up settings.²

Plain radiographs are ordered if a fracture, foreign body, septic joint, or tumor is suspected. If the initial films show no fracture but suspicion remains, films repeated in 1 to 2 weeks may show callus formation or abnormal alignment. Radiographic findings may also assist in diagnosing the type of arthritis (Box 107.5),³ although they may remain normal early in the course. The presence of degenerative changes in a painful joint supports the clinical suspicion of OA as the cause, but such changes also become common with age, even in asymptomatic joints; conversely, a normal film does not rule out OA. Similarly, calcified fibrocartilage is often found in patients with calcium pyrophosphate deposition (CPPD) disease but is common in asymptomatic patients as well. Ultrasonography is useful in confirming joint effusion, especially in joints that are difficult to assess, such as the hip. Other modalities are rarely indicated in the emergency department (ED). Although magnetic resonance imaging (MRI) can distinguish synovitis from effusion and identify rotator cuff tears or be used to evaluate ligament trauma, emergency MRI or computed tomography (CT) is indicated only if a severe joint complication is strongly suspected or if axial skeletal pain merits evaluation for stenosis or metastatic disease.

Arthrocentesis with synovial fluid analysis is an important diagnostic and therapeutic procedure for joint disease (see the Tips and Tricks box and Box 107.6). It is the only reliable means to rule out a septic joint, and it is essential in acute monarthritis to look for joint infection, crystals, or hemarthrosis. Possible complications of arthrocentesis include introduction of infection into the joint space, hemarthrosis, and adverse reactions to medications. Arthrocentesis of prosthetic joints is best done with orthopedic consultation.

Normal synovial fluid is clear and yellow in appearance. In degenerative joint disease the fluid itself is normal and thus remains clear. Bloody fluid suggests hemarthrosis. Fat droplets may confirm a fracture. Turbid fluid is observed in inflammatory conditions: gout, pseudogout, and septic, rheumatoid and seronegative arthritides (Table 107.2).

Crystal analysis is performed under compensated polarizing microscopy. In patients with acute gout, monosodium urate crystals are present inside neutrophils in fluid from the affected joint. The crystals are typically needle shaped and appear yellow when parallel to the compensator; this is negative birefringence. Sensitivity is at least 85%, and specificity for gout is 100%.⁴ In pseudogout, the crystals are positively birefringent (blue when parallel to the compensator), usually rhomboid shaped, and also phagocytized by neutrophils. Acute gouty arthritis may occasionally coexist with septic arthritis or pseudogout.

Glucose may be decreased relative to serum glucose in severe inflammatory disorders: down to less than 50% of the serum glucose level in septic arthritis and 50% to 75% in rheumatoid and seronegative arthritides. However, evidence suggests that chemistry studies on joint fluid should be discouraged because their results may be misleading or redundant.⁵

Viscosity can be measured grossly in the laboratory and ED. Inflammation decreases the hyaluronate portion of synovial fluid, and thus viscosity decreases. When dropped from a syringe, normal synovial fluid makes a 5- to 10-cm string of fluid before dropping. With inflammation, the string of fluid will be shorter or the fluid may simply form droplets.

Although a joint WBC count higher than 50,000/mm³ is generally said to be positive for infection, septic arthritis can occur with lower joint WBC counts, especially early in infection (36% of patients with septic arthritis had joint WBC counts lower than 50,000/mm³).⁶ In addition, patients with inflammatory arthritides such as RA, gout, and pseudogout may have very high joint WBC counts. Thus fluid must also be sent for Gram stain and culture. The yield is increased by immediate plating in the laboratory and perhaps by inoculating blood culture bottles with joint fluid in the ED. The serum WBC count, ESR, and joint WBC count are extremely variable in adults with septic arthritis.⁷ In the absence of a positive Gram stain, the ED clinician must consider the whole picture when determining the probability of septic arthritis.

Follow-up, Next Steps in Care, and Patient Education

Serious situations may warrant admission (Box 107.7). Patients with joint infections require admission and early consultation with an orthopedic surgeon or rheumatologist.

Most other patients will be discharged home with an analgesic and general treatment measures to relieve pain. Full-dose acetaminophen (650 to 1000 mg four times daily) may be adequate (especially if a history such as gastrointestinal [GI] bleeding, heart failure, or renal failure makes use of an NSAID risky), or an NSAID may be selected based on low cost and safety profile (e.g., celecoxib may be safer for the stomach). The NSAID is begun at a high dose (e.g., ibuprofen, 600 to 800 mg three times daily), continued for at least 2 to 3 days (or with inflammatory arthritis, for at least a few days after the pain stops), and then may be continued as needed. The patient is advised to take NSAIDs with food, especially with a history of stomach upset, and cotreatment with a stomach-protective drug (H₂ blocker, proton pump inhibitor, or sucralfate [Carafate]) should be considered. Nonresponders may be switched to a different NSAID, often with good relief, or may be given concomitant acetaminophen or tramadol. Judicious short-term use of narcotic analgesics is also helpful.

Topical analgesics may help, especially if only a single joint is problematic. Topical NSAIDs (diclofenac or ketoprofen, but not salicylates) and capsaicin (thin film of 0.025% cream applied four times per day) have been shown in trials to be beneficial, but maximal relief may take 3 to 4 weeks. Topical NSAIDs avoid the GI and renal complications of oral agents.^10,11 Lidocaine patches are another option, although unstudied.

General treatment measures should be recommended, including ice packs or heat (or both), temporary support (elastic wrap; brace, cane, or walker) and joint rest, but unnecessary or prolonged immobilization should be avoided. Patient education should include simple measures to avoid repetitive injury (e.g., patients with shoulder pain often ignore the obvious trigger of carrying a heavy shoulder bag). Simple splinting or ergonomic advice may assist patients with pain related to repetitive motions when the activity is unavoidable.

Appropriate lifestyle recommendations for patients with chronic arthritis are to stay as active as possible with daily activities and reasonable exercise programs. Physical and occupational therapy¹² may contribute greatly to improved quality of life and ability to maintain independence in self-care but are usually arranged by the continuity physician. Initial range-of-motion (ROM) and later strengthening and aerobic exercise regimens are recommended; swimming pool exercise programs are quite helpful. Obese patients with lower extremity arthritis should be educated about the importance of weight reduction.

Follow-up care includes referral to a primary care physician for most patients. Rheumatology referral is recommended for patients with clinical suspicion of new inflammatory or autoimmune arthritides such as RA or for patients not improving despite adequate general care. Chronic severe pain with significant disability merits orthopedic referral. Patient education is vital for achieving an optimal outcome (see the Patient Teaching Tips box).