Box 24.1 ETIOLOGY OF ACUTE MONOARTICULAR ARTHRITIS

EVALUATION OF A PATIENT WITH ACUTE MONOARTICULAR ARTHRITIS

HISTORY AND PHYSICAL EXAMINATION

Any acute inflammatory process that develops in a single joint over a few days (<2 weeks) is considered acute monoarticular arthritis. A careful history with emphasis on the chronology of symptoms may help in assessing the diagnosis of acute monoarticular arthritis. Historical features that should be sought include fever, rigors, recent sexual activity, gastrointestinal or genitourinary symptoms, recent illnesses, tick exposure, travel to an endemic area, past history of recurrent attacks, renal insufficiency, and a family history of gout or other arthritic conditions. Patients may note concurrent or preexisting involvement of other joints. Special attention should be paid to patients with rheumatoid arthritis (RA) who present with one joint that is significantly more painful and swollen than the rest of the other affected joints and those with a prosthetic joint, as these groups represent a high risk for septic arthritis.

    The physical examination should focus on determining whether the source of pain is in the true joint or periarticular soft tissues such as tendon, ligaments, or bursae. Asking the patient to point to the exact site of tenderness may be helpful. The joint should carefully be examined for warmth, erythema, and a possible effusion. Intra-articular involvement causes restriction of active and passive range of motion. Stress pain (maximum pain at limits of joint motion) is characteristic of true arthritis. Patients with a septic or crystalline arthritis will be exquisitely tender on examination of the joint. Specific maneuvers should assist in distinguishing true inflammatory arthritis from soft-tissue periarthritis or pain syndromes such as medial epicondylitis, bicipital or rotator cuff tendinopathy, trochanteric bursitis, and prepatellar and/or anserine bursitis. Joint effusion may not be readily visible on physical examination. In the knee joint, the “bulge sign” can signal a small effusion. Musculoskeletal ultrasound may assist the identification of small effusions not detected on clinical examination and facilitate evaluation of surrounding soft tissue. The physical examination should focus not only on inspection of the involved joint but also on other joints, as well as signs of an underlying systemic disorder. Involvement of fewer than four joints (oligoarticular) or more than four (polyarticular) would sway the diagnosis toward crystal arthritis or seronegative or seropositive RA rather than septic arthritis, or would portend a worse prognosis for a patient with polyarticular septic arthritis.

DIAGNOSTIC STUDIES

The diagnostic test for acute monoarticular arthritis is arthrocentesis of the affected joint for analysis of cell count, polarized microscopy, and culture of the synovial fluid. Diagnostic arthrocentesis is required in most patients presenting with a monoarthritis and a suspicion of infectious arthritis. Superimposed cellulitis is a relative contraindication to arthrocentesis. The procedure can safely be performed in patients who are anticoagulated (Coumadin) by using the smallest possible needle size or under ultrasound guidance. In some instances as little as one or two drops of synovial fluid may be aspirated in an initially presumed “dry tap,” with a priority placed in obtaining a Gram-stain culture and crystal analysis.

    Normal synovial fluid is colorless, and the gross appearance of the fluid can provide a clue to a possible noninflammatory versus inflammatory joint process as shown in Figure 24.1. Synovial fluid that is cloudy or purulent represents an inflammatory joint effusion. The presence of a bloody synovial effusion may represent a traumatic injury.

    Analysis of the cell count of synovial fluid will give more information about an inflammatory versus noninflammatory effusion and the likelihood of a septic joint (box 24.2). Noninflammatory effusions have a white blood cell (WBC) count <2000/mm³. An inflammatory synovial effusion will have a leukocyte count >2000 cells/mm³. WBC counts >100,000/mm³ are generally associated with a septic arthritis until proved otherwise, but can be seen with a variety of inflammatory disorders (i.e., gout, pseudogout, RA, and other inflammatory arthritis). Conversely, lower cell counts can be seen in patients with septic arthritis, especially with chronic atypical infections such as Mycobacterium or with partially treated infections. Although the cell count is useful in determining whether or not an effusion is inflammatory, a Gram stain and culture are required in all patients in whom septic arthritis is suspected.

Box 24.2 SYNOVIAL FLUID AND ASSOCIATED CONDITIONS

IMAGING STUDIES

Radiographs are of initial value, if significant trauma or focal bone pain is present, to exclude fracture, tumor, or osteomyelitis. However, they play no role in the initial distinction between acute crystal-induced or septic arthritis. Radiographs may confirm the presence of a joint effusion in joints where effusions are difficult to ascertain by physical examination (i.e., elbow, ankle, and hip). The presence of tophaceous erosions, chondrocalcinosis, and joint-space narrowing does not exclude the possibility of infection as an etiology of acute monoarthritis. Musculoskeletal ultrasound provides a simple technique not only to assess small effusions but also perform ultrasound-guided arthrocentesis of the affected joints. Computed tomography (CT) scans should be reserved to detect effusions and needle placement for aspirations of joints that are difficult to assess, such as the hip, sacroiliac, or sternoclavicular joints. Magnetic resonance imaging (MRI) demonstrates adjacent soft tissue edema or abscess and may be helpful in detecting septic sacroiliitis.

SYNOVIAL BIOPSY AND ARTHROSCOPY

Needle biopsy of the synovial membrane under ultrasound or biopsy obtained during arthroscopy are seldom performed as part of the initial evaluation of monoarticular arthritis. In rare instances synovial biopsy may assist in the diagnosis of refractory monoarthritis such as that seen with atypical infectious agents (e.g., tuberculosis or fungal infections), infiltrative diseases (e.g., amyloidosis), sarcoidosis, pigmented villonodular synovitis (PVNS), or intra-articular tumors.

DIFFERENTIAL DIAGNOSIS

Acute monoarthritis can have many causes (box 24.1), but crystals, trauma, and infection are most common. Prompt diagnosis of joint infection is critical because of its destructive nature. An algorithm for evaluation of patients who present with acute monoarticular arthritis is outlined in Figure 24.2. The crystal-induced arthritides are the most important forms of acute arthritis that are difficult to differentiate from acute monoarticular septic arthritis on clinical examination. Any form of chronic inflammatory joint disease such as a reactive arthritis (ReA), psoriatic arthritis (PsA), spondyloarthropathy (SpA), and arthritis associated with inflammatory bowel disease (IBD) can present with a swollen joint that simulates septic arthritis. Most patients with these conditions have extra-articular manifestations of their disease, such as recent genitourinary or gastrointestinal symptoms, conjunctivitis or uveitis, enthesopathy, or skin or mucous membrane lesions, with a predilection for lower back pain, and stiffness or sacroiliac joint involvement. Another rheumatic disease that is important to differentiate from septic arthritis is RA. Although the clinical presentation of RA is a symmetric, chronic, polyarticular joint disorder, some patients may present with an acute or subacute exacerbation of one or few of their joints. One-third of the patients with RA may present with monoarticular arthritis as their initial presentation. They may present with a pseudo–septic arthritis picture, including an explosive synovitis with marked synovial fluid leukocytosis. Similarly, RA patients on biological therapy may present with monoarthritis not related to RA flares but to underlying septic arthritis, highlighting the importance of a Gram stain and culture of the synovial fluid. Other mimickers of septic arthritis include subacute bacterial endocarditis and any periarticular inflammation.

SEPTIC ARTHRITIS

Normal, diseased, and prosthetic joints are all vulnerable to bacterial infection (box 24.3). Acute bacterial arthritis remains a medical emergency with significant morbidity and mortality even when proper antibiotic therapy is instituted; therefore, timely recognition is imperative for a favorable outcome. There are two peaks of incidence that seem to be age dependent: one under the age of 15 and the other over the age of 55 years. The mortality rates in adults ranges from 10% to >50%. More than 30% of patients will be left with some irreversible residual joint damage. As with any monoarticular arthritis, a thorough history and physical examination remain key to diagnosing septic arthritis.

Box 24.3 THE INFECTING BACTERIA IN NORMAL, DISEASED, AND PROSTHETIC JOINTS

PATHOGENESIS

The synovium is highly vascular and contains no limiting basement membrane, promoting easy access of blood contents to the synovial space. Most acute septic arthritis results from seeding of the joint through four possible entry routes: most commonly through hematogenous or contiguous spread of the organism, sometimes by penetrating trauma, and rarely by iatrogenic joint injection. Any infection that affects the skin, soft tissues, or mucous membranes (respiratory, gastrointestinal, or genitourinary tracts) can seed a joint through the bloodstream. Localized infections from an adjacent focus can also spread contiguously into the joint space. Direct inoculation can occur with any penetrating trauma or any procedural invasion of the joint space, such as with an arthrocentesis or arthroscopy. Once the bacteria enter the closed joint space, they can trigger an acute inflammatory response within a few hours. The synovial membrane reacts with proliferative hyperplasia and an influx of acute and chronic inflammatory cells, creating the characteristic acute purulent joint inflammation. In a few days the inflammatory cells release various cytokines and proteases, leading to cartilage damage, inhibition of cartilage synthesis, irreversible bone loss, and joint damage.

MICROBIOLOGY

Septic joint effusions may be due to bacteria, mycobacteria, or fungi. The most common etiology for joint infection is the gram-positive cocci, either staphylococci or streptococci. Staphylococcus aureus is the most frequent cause in joint infection, including both native and prosthetic joints, although Staphylococcus epidermidis occurs more commonly in prosthetic joints. Gram-negative bacilli are seen in 5–20% of patients and usually occur in elderly adults, those with comorbidities, or intravenous drug abusers, or both. Anaerobic organisms rarely cause septic arthritis; however, they can be seen in any penetrating trauma. Neisseria gonorrhoeae is the most common sexually transmitted organism causing infectious arthritis, and although it used to be a common cause for infectious arthritis in the 1970s and 1980s, the incidence has now decreased significantly.

RISK FACTORS

Experimental evidence suggests that normal joints are very resistant to infection compared with diseased or prosthetic joints. Systemic, local, and social factors are important risk factors that contribute to the risk of developing bacteremias and reduce the body’s capacity to eliminate organisms from the joint (box 24.4). Systemic disorders affect the host’s response through an impaired immune system. Local factors such as damage to a specific joint from earlier trauma, recent joint surgery or arthroscopy, and the presence of a prosthetic joint are important predisposing factors for septic arthritis. Social factors include occupational exposure to animals (e.g., brucellosis), exposure to tuberculosis, mass emigration from endemic areas of the world, and factors that lead to an immunocompromised state (AIDS, intravenous drug abuse [IVDA], homelessness, therapeutic noncompliance, and emergence of drug-resistant mycobacteria). In some cases, the risk factors are compounded by medications (e.g., patients with RA or inflammatory arthritis treated with immunosuppressant, anti-tumor necrosis factor-α [TNF-α] therapy, and steroids). Furthermore, it may also be difficult to distinguish an infectious etiology in patients receiving immunosuppressive therapy. Risk factors for increased mortality in septic arthritis include age >65, mental status changes at presentation, multiple joint involvement, and systemic symptoms (suggesting a higher bacterial load).

Box 24.4 PREDISPOSING FACTORS IN BACTERIAL ARTHRITIS

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