Infections of the joint are most commonly bacterial but may be caused by an array of organisms (fungal, mycobacterial, or viral). The term septic arthritis encompasses bacterial arthritis, pyogenic arthritis, suppurative arthritis, purulent arthritis, and pyarthrosis. Primary septic arthritis is a result of hematogenous (most common) or direct inoculation. Secondary septic arthritis results from the spread of osteomyelitis into an adjacent joint, typically through the intracapsular portion of the metaphysis in joints like the hip, shoulder, elbow, or ankle.¹ Infections of the knee (most common), hip, and ankle account for at least 80% of cases. Early diagnosis and treatment of a septic hip is essential in preserving function. Delay in treatment increases the risk of complications, including osteonecrosis of the capital femoral epiphysis, osteomyelitis, chondrolysis, sepsis, and chronic osteoarthritis.

Septic arthritis occurs most commonly in children younger than 3 years of age, and boys more often than girls (male-to-female ratio of 1.2–2:1). Staphylococcus aureus is the dominant causative agent of infection^1,2 (see Table 62-1 for causative organisms). The prevalence of community-acquired methicillin-resistant S. aureus (CA-MRSA) is rising, with reports of a three- to tenfold increase in septic arthritis and acute osteomyelitis since the beginning of this century. Various reports from urban pediatric centers across the North America have documented not only a rising incidence, but also more extensive local soft-tissue destruction, more rapid spread of infection, and a higher overall mortality rate.^2–4 Studies have shown that CA-MRSA leads to an increased length of hospital stay and increased complications (i.e., persistent bacteremia, DVT, septic pulmonary emboli), greater need for surgical intervention, admission to an ICU for circulatory compromise, and residual morbidities.^2–4

K. kingae, a gram-negative coccobacillus, is emerging as a common cause of osteoarticular infections. K. kingae may account for as many as 50% of septic arthritis cases in children younger than 2 years of age. Patients with K. kingae appear only mildly ill and have normal or modest elevations in inflammatory markers (erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]). There is evidence that K. kingae first colonizes the oropharynx before penetrating the bloodstream and invading distant organs. Polymerase chain reaction (PCR) testing is promising as a supplemental tool to increase the rate of identification of the causative organism in septic arthritis.^5,6 Ceroni et al. demonstrated that an oropharyngeal swab PCR, specific to the K. kingae RTX toxin can be used when considering K. kingae as the organism responsible for an osteoarticular infection, or even stronger evidence that it is not, if culture negative.^6,7 In Lyme-endemic areas, children with late-onset Lyme disease may present with a more indolent form of septic arthritis, often months after exposure and with minimal to no associated systemic illness, a propensity for knee involvement, and lower inflammatory markers than other infectious causes.⁸

PATHOPHYSIOLOGY

Normal joints contain a small amount of synovial fluid, which is viscous, clear, and mostly acellular. Microorganisms can enter the joint space by hematogenous spread (which accounts for most cases), direct inoculation, or extension of a contiguous focus of infection (i.e., osteomyelitis). The high, effective blood flow and lack of basement membrane in the synovium facilitate the entry of bacteria into the joint space during episodes of bacteremia. Host cells respond to bacterial endotoxin with a release of cytokines, which promote increased levels of proteolytic enzymes and increase leukocyte migration. This results in joint damage from destruction of the synovium and collagen matrix, and inhibition of cartilage synthesis.

HISTORY AND PHYSICAL EXAMINATION

Obtain a history and physical examination when evaluating a child with possible joint pain to narrow the differential diagnosis. The physical exam findings vary based on the stage of the infection and organism. The most frequent clinical findings include fever (95%), pain (80%), localized signs and symptoms (70%), reduced range of movement (50%), and reduced weight-bearing (50%).⁵ Adapt clinical tests to identify the source of pain as intra-articular or extra-articular. The flexion-abduction-external rotation (FABER), internal range of motion with overpressure (IROP), and scouring (quadrant) tests are useful in identifying individuals with intra-articular pathology (see also Chapter 109).

When evaluating a child for suspected septic arthritis, the knee and ankle joints are typically swollen, red, warm, and tender to palpation. Active and passive range of motion of the hip is usually decreased and painful. Pain increases with maneuvers that increase intracapsular pressure (e.g., compression of the head of the femur into the acetabulum). When septic arthritis of the hip is suspected, there is often a history of nontraumatic progressive pain in the hip, limp, fever, and irritability. In the infant, asymmetric buttock creases or swelling of the buttock or the genitalia may be present with unilateral hip involvement. Pseudoparalysis, or inability to move an extremity, is a common finding of bone and joint involvement in the young infant. See Table 62-2 for signs and symptoms.

Severe symptoms do not always imply severe disease, as toxic synovitis can immobilize the hip with pain but is a benign and self-limited condition (see Chapter 111). Do not discharge a child who is unable to bear weight in the ED until a diagnosis is made and therapy instituted.

DIAGNOSTIC EVALUATION

Conduct a laboratory evaluation of a child in whom you suspect septic arthritis with a complete blood count (CBC) with differential, acute phase reactants (ESR and CRP), and blood culture (BC).^9–12 Obtain synovial fluid through arthrocentesis for Gram stain, culture (aerobic and anaerobic with susceptibility testing), white blood cell (WBC) count with differential, and may also relieve pain by decompressing the joint space (see Chapter 109). Hold additional fluid, if available, for PCR testing to help with identification in partially treated cases or when no organism is recovered by routine cultures after several days. For hip involvement, obtain radiographs with the child in the frog-leg position (femur externally rotated, flexed, and abducted). Early radiographic findings of septic arthritis include widening of the joint space, subluxation, and soft-tissue swelling. Late findings include erosion of the epiphyses and erosion of adjacent subchondral bone (indicative of concurrent osteomyelitis). Use ultrasound to guide diagnostic aspiration. Lack of visualized fluid has a high negative predictive value. The sonographic characteristics of the fluid (i.e., echolucent vs. echogenic) do not correlate with infection, but ultrasound can discern cartilaginous structures.

MRI is highly sensitive for the early detection of joint fluid, and can demonstrate abnormalities of adjacent bone and soft tissue, the extent of cartilage destruction, and concomitant osteomyelitis or osteomyelitis-associated abscess.^13–14 Given the high incidence of coexisting osteomyelitis with septic arthritis, evidence and expert opinion usually recommend MRI rather than ultrasound alone when clinically feasible.¹²

TRANSIENT/TOXIC SYNOVITIS

Transient synovitis (also known as toxic synovitis) is an inflammation of the synovium that can occur in any large joint but is most common in the hip. Transient synovitis typically occurs in children between the ages of 3 and 8 years, with a mean age at presentation of 5 to 6 years. The incidence is 0.2%, with a 2:1 male-to-female ratio. Often, patients with transient synovitis have a history of a preceding upper respiratory tract infection. When the hip is involved, physical examination reveals a limping child who has decreased internal rotation of the hip.¹ Patients with transient synovitis often have a less severe clinical presentation (less pain and lower fever) compared with patients who have septic arthritis. Transient synovitis, in contrast to septic arthritis, is self-resolving; manage with nonsteroidal anti-inflammatory agents and return to full activity as tolerated within 1 to 2 weeks. It remains the most prevalent disease process in the differential diagnosis of musculoskeletal infections in childhood.

The Kocher criterion is a tool useful in the differentiation between septic arthritis and transient synovitis of the hip, and has been successfully applied in other anatomic locations. The four clinical predictors initially described to distinguish septic arthritis from transient synovitis were a history of fever (>38.5^oC), non–weight-bearing status (inability to bear weight even with support), an ESR greater than 40 mm/hr, and a serum WBC count greater than 12,000 cells/mm³.^9–10 In 2006, Caird et al. added CRP >2 mg/dL (>20 mg/L) to the predictive model, and showed its strength as an independent predictor. Prior studies have specifically shown CRP as a useful negative predictor when normal. Although there is no perfect clinical model to predict septic arthritis, the greater number of clinical and laboratory factors that are positive, the higher the likelihood of septic arthritis¹¹ (Table 62-3).^9–12

TREATMENT AND OUTCOME

Treatment of septic arthritis is time-sensitive. The release of proteolytic enzymes in the joint leads to articular damage within 8 hours of onset, increasing intracapsular pressure, which ultimately may cause venous stasis and osteonecrosis.¹ Treat septic arthritis primarily with early empiric antibiotic therapy and drainage with irrigation. Specific microbiological confirmation of infection often is not achieved; therefore do not significantly delay treatment once initial cultures are obtained, especially in systemically ill children. Treat with sterilization and decompression of the joint space and removal of inflammatory debris to relieve pain and prevent deformity or functional sequelae. Drainage can be accomplished through needle aspiration or open surgery (arthrotomy). Delayed drainage increases the likelihood of adverse outcome. Length of IV antibiotics varies between 2 and 6 weeks, with growing evidence in support of shortening such a regimen and transition to oral antibiotics as one sees substantial clinical improvement, decrease in inflammatory markers, and a resolution of systemic symptoms¹⁵ (Tables 62-4 and 62-5).