Septic Arthritis

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Chapter 677 Septic Arthritis

Septic arthritis in infants and children has the potential to cause permanent disability. Early recognition of septic arthritis in young patients before extensive infection develops and prompt institution of appropriate medical and surgical therapy minimize further damage to the synovium, adjacent cartilage, and bone.

Etiology

Historically, Haemophilus influenzae type b (Chapter 186) accounted for more than half of all cases of bacterial arthritis in infants and young children. Since the development of the conjugate, it is now a rare cause; Staphylococcus aureus (Chapter 174.1) has emerged as the most common infection in all age groups. Methicillin-resistant S. aureus accounts for a high proportion (>25%) of community S. aureus isolates in many areas of the USA and throughout the world. Group A streptococcus (Chapter 176) and Streptococcus pneumoniae (pneumococcus) (Chapter 175) historically cause 10-20%; S. pneumoniae is most likely in the first 2 years of life. Kingella kingae is recognized as a relatively common etiology with improved culture and polymerase chain reaction (PCR) methods in children <5 yr old (Chapter 676). In sexually active adolescents, gonococcus (Chapter 185) is a common cause of septic arthritis and tenosynovitis, usually of small joints or as a monoarticular infection of a large joint (knee). Neisseria meningitidis (Chapter 184) can cause either a septic arthritis that occurs in the first few days of illness or a reactive arthritis that is typically seen several days after antibiotics have been initiated. Group B streptococcus (Chapter 177) is an important cause of septic arthritis in neonates.

Fungal infections usually occur as part of multisystem disseminated disease; Candida arthritis can complicate systemic infection in neonates with or without indwelling vascular catheters. Primary viral infections of joints are rare, but arthritis accompanies many viral (parvovirus, mumps, rubella live vaccines) syndromes, suggesting an immune-mediated pathogenesis.

A microbial etiology is confirmed in about 65% of cases of septic arthritis. Prior antibiotic therapy and the inhibitory effect of pus on microbial growth might explain the low bacterial yield. Additionally, some cases treated as bacterial arthritis are actually postinfectious (gastrointestinal or genitourinary) reactive arthritis (Chapter 151) rather than primary infection. Lyme disease produces an arthritis more like a rheumatologic disorder and not typically suppurative.

Clinical Manifestations

Most septic arthritides are monoarticular. The signs and symptoms of septic arthritis depend on the age of the patient. Early signs and symptoms may be subtle, particularly in neonates. Septic arthritis in neonates and young infants is often associated with adjacent osteomyelitis caused by transphyseal spread of infection, although osteomyelitis contiguous with an infected joint can be seen at any age (Chapter 676).

Older infants and children might have fever and pain, with localizing signs such as swelling, erythema, and warmth of the affected joint. With involvement of joints of the pelvis and lower extremities, limp or refusal to walk is often seen.

Erythema and edema of the skin and soft tissue overlying the site of infection are seen earlier in septic arthritis than in osteomyelitis, because the bulging infected synovium is usually more superficial, whereas the metaphysis is located more deeply. Septic arthritis of the hip is an exception because of the deep location of the hip joint.

Joints of the lower extremity constitute 75% of all cases of septic arthritis (Table 677-1). The elbow, wrist, and shoulder joints are involved in about 25% of cases, and small joints are uncommonly infected. Suppurative infections of the hip, shoulder, elbow, and ankle in older infants and children may be associated with an adjacent osteomyelitis of the proximal femur, proximal humerus, proximal radius, and distal tibia because the metaphysis extends intra-articularly.

Table 677-1 ANATOMIC DISTRIBUTION OF SEPTIC ARTHRITIS

BONE %
Knee ∼40
Hip 22-40
Ankle 4-13
Elbow 8-12
Wrist 1-4
Shoulder ∼3
Interphalangeal <1
Metatarsal <1
Sacroiliac <1
Acromioclavicular <1
Metacarpal <1
Toe ∼1

Modified from Gafur OA, Copley LA, Hollmig ST, et al: The impact of the current epidemiology of pediatric musculoskeletal infection on evaluation and treatment guidelines, J Pediatr Orthop 28:777–785, 2008.

Diagnosis

Blood cultures should be performed in all cases of suspected septic arthritis. Aspiration of the joint fluid for Gram stain and culture when the history and physical findings indicate septic arthritis remains the definitive diagnostic technique and provides the optimal specimen for culture to confirm the diagnosis. Most large joint spaces are easy to aspirate, but the hip can pose technical problems; ultrasound guidance facilitates aspiration. Aspiration of joint pus provides the best specimen for bacteriologic culture of infection. If gonococcus is suspected, cervical, anal, and throat cultures should also be obtained. In addition to prompt inoculation onto solid media, inoculation of the specimen in blood culture bottles can increase recovery of K. kingae. PCR appears to be the most sensitive method for detecting K. kingae in joint fluid.

Synovial fluid analysis for cell count, differential, protein, and glucose has limited usefulness because noninfectious inflammatory diseases, such as rheumatic fever and rheumatoid arthritis, can also cause exuberant reaction with increased cells and protein and decreased glucose. Nevertheless, cell counts >50,000-100,000 cells/mm3 generally indicate an infectious process. Synovial fluid characteristics of septic arthritis can suggest infection but are not sufficiently specific to exclude infection.

The white blood cell count and differential, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) are generally elevated in children with joint infections but are nonspecific and might not be helpful in distinguishing between infection and other inflammatory processes. The leukocyte count and ESR may be normal during the first few days of infection, and normal test results do not preclude the diagnosis of septic arthritis. Monitoring elevated ESR and CRP may be of value in assessing response to therapy or identifying complications.

Radiographic Evaluation

Radiographic studies play a crucial role in evaluating septic arthritis. Conventional radiographs, ultrasonography, CT, MRI, and radionuclide studies can all contribute to establishing the diagnosis (Fig. 677-1).

image

Figure 677-1 MRI of staphylococcal septic arthritis of left hip, with fluid collections between planes of gluteal muscles. Arrows indicate fluid collection.

(From Matthews CJ, Weston VC, Jones A, et al: Bacterial septic arthritis in adults, Lancet 375:846–854, 2010.)

Treatment

Optimal treatment of septic arthritis requires cooperation of pediatricians, orthopedic surgeons, and radiologists to benefit the patient.

Antibiotic Therapy

The initial empirical antibiotic therapy is based on knowledge of likely bacterial pathogens at various ages, the results of the Gram stain of aspirated material, and additional considerations. In neonates, an antistaphylococcal penicillin, such as nafcillin or oxacillin (150-200 mg/kg/24 hr divided q6h IV), and a broad-spectrum cephalosporin, such as cefotaxime (150-225 mg/kg/24 hr divided q8h IV), provide coverage for the S. aureus, group B streptococcus, and gram-negative bacilli. If MRSA is a concern, vancomycin is selected in favor of nafcillin or oxacillin. If the neonate is a small premature infant or has a central vascular catheter, the possibility of nosocomial bacteria (Pseudomonas aeruginosa or coagulase-negative staphylococci) or fungi (Candida) should be considered.

In older infants and children with septic arthritis, empirical therapy to cover for S. aureus, streptococci, and K. kingae includes cefazolin (100-150 mg/kg/24 hr divided q8h) or nafcillin (150-200 mg/kg/24 hr divided q6h).

In areas where methicillin resistance is noted in ≥10% of community S. aureus strains (CA-MRSA), including an antibiotic that is effective against CA-MRSA isolates is suggested. Clindamycin (30-40 mg/kg divided q8h) and vancomycin (15 mg/kg q6-8h IV) are alternatives when treating CA-methicillin-resistant S. aureus infections. For immunocompromised patients, combination therapy is usually initiated, such as with vancomycin and ceftazidime or with extended-spectrum penicillins and β-lactamase inhibitors with an aminoglycoside. Adjunct therapy with dexamethasone for 4 days with antibiotic therapy appeared to benefit children with septic arthritis in one study but has not been studied in children with CA-MRSA septic arthritis.

When the pathogen is identified, appropriate changes in antibiotics are made, if necessary. If a pathogen is not identified and a patient’s condition is improving, therapy is continued with the antibiotic selected initially. If a pathogen is not identified and a patient’s condition is not improving, re-aspiration or the possibility of a noninfectious condition should be considered.

Duration of antibiotic therapy is individualized depending on the organism isolated and the clinical course. Ten to 14 days is usually adequate for streptococci, S. pneumoniae, and K. kingae; longer therapy may be needed for S. aureus and gram-negative infections. Normalization of ESR and CRP in addition to a normal examination supports discontinuing antibiotic therapy. In selected patients, obtaining a plain radiograph of the joint before completing therapy can provide evidence (typically periosteal new bone) of a previously unappreciated contiguous site of osteomyelitis that would likely prolong antibiotic treatment. Oral antibiotics can be used to complete therapy once the patient is afebrile for 48-72 hr and is clearly improving.

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