Essentials of Diagnosis

• The classic presentation is acute onset of painful, warm, and swollen joint, usually monoarticular and affecting large weight-bearing joints.
  
• Synovial fluid white blood cell counts usually >50,000 cells/mcL with over 80% neutrophils.
  
• Positive synovial fluid culture.
  
• Staphylococcus aureus is the most common cause of septic arthritis in native joints.

General Considerations

The reported incidence of septic arthritis varies from 2–10 per 100,000 per year in the general population, with substantially higher rates in patients with rheumatoid arthritis (RA) or joint prostheses (both ∼30–70 cases per 100,000 per year). The incidence of bacterial arthritis is significantly higher among children than adults.

Septic (bacterial) arthritis is a medical emergency, and delay in diagnosis and treatment can lead to irreversible joint destruction and an increase in mortality. Even with the advent of better antimicrobial agents and techniques of joint incision and drainage, the rate of permanent joint damage from septic arthritis is 25–50%. The case fatality rate for monoarticular bacterial arthritis also remains high at 11%, with increased mortality rates seen in the setting of polyarticular septic arthritis (as high as 50%), underlying RA, and in immunocompromised states. Risk factors for the development of bacterial arthritis include chronic arthritic syndromes, prosthetic joints, parenteral drug use, extremes of age, diabetes mellitus, and immunocompromised conditions (Table 47–1).

Pathogenesis

Bacterial pathogens reach the joint spaces by hematogenous spread (>50% of cases), direct inoculation, or spread from adjacent bony or soft-tissue infections. The lack of a limiting basement membrane and high vascularity of the synovium allows for easy bacterial access. Although skin infections are the most common predisposing infections to joint infections, transient bacteremia from respiratory, gastrointestinal, or genitourinary infections can also lead to septic arthritis. Bacteria enter the closed joint space, and within hours the synovium becomes infected, leading to synovial membrane proliferation and infiltration by polymorphonuclear and other inflammatory cells. This inflammatory response in turn leads to enzymatic and cytokine-mediated degradation of the articular cartilage, neovascularization, and the eventual development of granulation tissue. Without appropriate treatment, irreversible subchondral bone loss and cartilage destruction occur within a few days of the initial infection.

Clinical Findings

Symptoms and Signs

The classic presentation of bacterial arthritis is the abrupt onset of a painful, warm, and swollen joint. More indolent presentations are seen in patients with preexisting rheumatic illnesses or immunocompromised states. An obvious joint effusion, moderate to severe joint tenderness to palpation, and marked restriction of both passive and active motion are common signs of septic arthritis.

A patient with an acute monoarticular arthritis should be considered to have septic arthritis until proven otherwise. Nongonococcal bacterial arthritis is monoarticular in 80–90% of cases, with polyarticular involvement (10–20%) carrying a poorer chance of survival. Polyarticular septic arthritis is more likely to occur in patients with RA or other systemic connective tissue diseases or in the syndrome of overwhelming sepsis. Infectious monoarthritis typically involves the knee (40–50%), hip (13–20%), shoulder (10–15%), wrist (5–8%), ankle (6–8%), elbow (3–7%), and the small joints of the hand or foot (5%). Bursitis, especially olecranon and prepatellar, may be the first manifestation of septic arthritis in patients with RA.

Septic arthritis manifests with fever in 60–80% of cases, although the temperature elevation is not usually pronounced. Twenty percent of patients with fever have shaking chills that usually correspond to waves of bacteremia. Cough, gastrointestinal symptoms, or dysuria may represent symptoms of the antecedent infection. Indeed, a preceding source of infection, such as pneumonia, otitis, bronchitis, pharyngitis, or cutaneous, gastrointestinal, or genitourinary infection, can be identified in up to 50% of septic arthritis cases.

Physical Examination

The initial physical examination for septic arthritis should determine whether the source of inflammation and pain is articular or periarticular (specifically, localized to skin, bursae, or tendons). Septic arthritis produces warmth, swelling, and tenderness of the involved joint, and attempts at passive and active motion of the joint usually produce considerable discomfort. Similar findings occur in noninfectious forms of severe inflammatory arthritis, such as acute gout. In contrast, cellulitis and inflammation of bursae and tendons do not cause joint effusions, and passive motion of the adjacent joint usually does not elicit severe pain unless there is stretching of an inflamed tendon. Because septic arthritis can involve more than one joint, all joints should be examined for warmth, swelling, deformity, range of motion, pain on motion, and tenderness.

Septic arthritis of the sacroiliac (SI) joint is often difficult to distinguish from infection in the hip because both present with fever and pain upon ambulation and because examination of the SI joints is difficult (see Chapter 1). Moreover, findings of SI septic arthritis can be subtle and can be mistaken for the syndrome of a protruded disk or a paraspinous muscular strain. Similarly, infection of the shoulder joint is often difficult to identify given the usual lack of a visible effusion. Adults with shoulder infections tend to be elderly, with multiple risk factors for the development of septic arthritis. Infections of the sternoclavicular joint most often occur in injection drug users; an abscess of the chest wall or mediastinitis will develop in 20% of patients with septic arthritis of the sternoclavicular joint. Septic olecranon bursitis is distinguished from infection of the elbow joint by the presence of swelling and erythema overlying the olecranon process and the absence of joint pain with passive extension of the elbow. Infection of the olecranon bursa often follows minor trauma to the region, which leads to inoculation of organisms (usually S aureus) into the bursal space.

Laboratory Findings

Peripheral Counts and Cultures

Peripheral white blood cell (WBC) counts are elevated in bacterial arthritis approximately two thirds of the time. The erythrocyte sedimentation rate and C-reactive protein are usually elevated and may be useful to monitor during treatment, however, they can also be elevated in other noninfectious arthropathies. Approximately 40–50% of patients with septic arthritis have associated bacteremia, so blood cultures should be obtained prior to the administration of antibiotics. Targeted cultures from extra-articular sites, such as respiratory, cutaneous, gastrointestinal, or genitourinary sites, should also be collected after a careful history and physical examination.

Synovial Fluid Analysis

Synovial fluid analysis is critical for the definitive diagnosis of septic arthritis. Synovial fluid is usually obtained by emergent arthrocentesis, with fluoroscopic, computed tomographic (CT), or ultrasonographic guidance if necessary (see Chapter 2). An open surgical procedure may be required to obtain synovial fluid and biopsies of the synovial membrane for the diagnosis of bacterial arthritis, especially in suspected sternoclavicular, hip, or shoulder infections or in the presence of prosthetic joints. Of note, arthrocentesis is contraindicated if the needle must pass through an area of cellulitis, heavily colonized skin lesions (eg, psoriatic plaques), or infection of any kind because of the risk of introducing bacteria into the joint space. Bacteremia is also a relative contraindication for the performance of arthrocentesis.

Once synovial fluid has been collected, the following analyses should be performed (see Chapter 2):

• Appearance: Look for color and clarity of the fluid, since purulence or turbidity or both suggest a septic process.
  
• Cell count and differential: The joint fluid in nongonococcal septic arthritis has more than 50,000 WBC/mcL in 50–70% of cases. Low synovial fluid cell counts may be seen early in the process of infectious arthritis, in the setting of partially treated infections, or in immunosuppressed patients. The majority of WBCs in infected synovial fluid are neutrophils (usually >80% polymorphonuclear cells).
  
• Gram stain for organisms: A positive Gram stain is diagnostic for septic arthritis (highly specific), but a Gram stain that is negative for bacteria does not rule out an infected joint. The Gram stain is positive 50–75% of the time in nongonococcal bacterial arthritis, with gram-positive bacterial arthritis more likely to stain positive than gram-negative bacterial arthritis. The Gram stain should be used to guide presumptive therapy.
  
• Culture: Bacterial culture of the synovial fluid is positive in 70–90% of cases of nongonococcal arthritis, depending on the organism. Inoculating synovial fluid into blood culture bottles rather than solid media increases the yield of culture growth and decreases the contamination rate.
  
• Microbiology: Table 47–2 shows the typical pathogens of nongonococcal bacterial arthritis and risk factors for their acquisition. S aureus is the most common cause of septic monoarthritis in native joints (60–70%) (Figure 47–1). The remaining causes of septic arthritis include streptococcal species, gram-negative rods, and anaerobes in relatively constant proportions. Hematogenous infection can result from transient bacteremia secondary to a remote infection or a surgical procedure, including dental work or respiratory, gastrointestinal, or genitourinary manipulations. Group A streptococci are often isolated from the infected joint after procedures in the oral cavity, whereas gastrointestinal procedures can lead to bacteremia with non–group A streptococcal species, gram-negative bacilli, or anaerobes.