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Bacterial arthritis: Clinical features and diagnosis in infants and children

Bacterial arthritis: Clinical features and diagnosis in infants and children
Literature review current through: Jan 2024.
This topic last updated: Apr 04, 2023.

INTRODUCTION — Infections of the joints (known as septic arthritis, pyogenic arthritis, suppurative arthritis, purulent arthritis, or pyarthrosis) may be caused by bacteria, fungi, mycobacteria, and viruses. The term "septic arthritis" usually refers to bacterial arthritis or fungal arthritis, but bacterial joint infections are most common [1,2].

The clinical features and diagnosis of bacterial arthritis in infants and children will be reviewed here. The epidemiology, pathogenesis, microbiology, treatment, and outcome of bacterial arthritis in infants and children are discussed separately. (See "Bacterial arthritis: Epidemiology, pathogenesis, and microbiology in infants and children" and "Bacterial arthritis: Treatment and outcome in infants and children".)

CLINICAL FEATURES

Classic presentation — Bacterial arthritis classically presents with acute onset (two to five days) of fever and joint pain, swelling (picture 1A-B), and limited range of motion. However, the presentation varies depending upon the age of the child, the site of infection, and the causative organism (table 1).

Bacterial arthritis usually occurs in a single joint, most commonly of the lower extremity [2]. Infections of the knee, hip, and ankle consistently account for at least 80 percent of cases, with the hip and knee most commonly affected [3]. Bilateral bacterial arthritis of the hip occurs in a small number of cases [4].

Up to 10 percent of cases involve more than one joint [5-7]. Polyarticular infections are more common in neonates and with certain pathogens (eg, Neisseria meningitidis, Neisseria gonorrhoeae, and occasionally Staphylococcus aureus) [6,8,9].

Concomitant osteomyelitis may be present, particularly in patients with pain for >4 days before presentation [10,11].

Neonates and infants

Typical presentation — In neonates and young infants (<2 to 3 months), the typical presentation of bacterial arthritis is that of septicemia (eg, irritability, poor feeding), cellulitis, or fever without a focus of infection [1]. Subtle features of joint involvement may include lack of use of the involved extremity ("pseudoparalysis"), aversion to or apparent discomfort on being handled (eg, being picked up, having the diaper changed), postural changes (eg, positional preferences), and unilateral swelling of the extremity, buttocks, or genitalia.

Bacterial arthritis in neonates and young infants deserves special attention for a number of reasons [8,12-15]:

The signs and symptoms can be subtle

More than one joint may be involved

The different microbiology (eg, group B Streptococcus, N. gonorrhoeae, and gram-negative enteric bacilli in addition to S. aureus) compared with older children

The potentially catastrophic consequences of untreated disease, particularly when the hip is involved (see "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Outcome')

Hip arthritis — Clinical features of bacterial arthritis of the hip in neonates and young infants may include [4,13,15]:

Swelling in the region of the thigh or buttock

Holding the leg flexed with slight abduction and external rotation

Irritability on passive movement of the hip (eg, during diaper change)

History of femoral venipuncture (usually 5 to 9 days before bacterial arthritis, but may be as recent as 1 day or as remote as 28 days before) [16,17]

Left untreated, bacterial arthritis of the hip may spontaneously drain along the obturator internus, manifesting as a lower-abdominal mass just above the inguinal canal [18].

Older children and adolescents — In addition to swelling, tenderness, and limited mobility of the affected joint, older children and adolescents with bacterial arthritis usually have fever and constitutional symptoms (malaise, poor appetite, irritability, tachycardia) within the first few days of infection [1,9,19]. Although these findings are not always present, bacterial arthritis should be considered seriously in all children with the acute onset of fever and joint pain and/or loss of function, such as limping.

Pain with active or passive movement is a cardinal feature, but findings related to the involved joint may be subtle. When bacterial arthritis involves the lower extremity or sacroiliac joint, children may present with limp or refusal to walk or bear weight.

When the hip or sacroiliac joint is involved, the pain maybe referred to adjacent structures [20-23]. For example, patients with an infection of the hip may complain of knee pain.

Bacterial arthritis of the sacroiliac joint usually occurs in late childhood (average age of 10 years) [22].Affected patients typically complain of pain in the buttock, but they may also have symptoms that mimic appendicitis, pelvic neoplasm, or urinary tract infection [22]. Young children with bacterial arthritis of the sacroiliac joint may refuse to sit [24].

Children with underlying arthritis — Bacterial arthritis should be considered as a possibility in children and adolescents with underlying juvenile idiopathic arthritis (formerly juvenile rheumatoid arthritis) if there is unusual worsening of one joint during an exacerbation of arthritis or there has been a recent injection of the joint in question.

EVALUATION

Timing and goals — The evaluation of infants and children with suspected bacterial arthritis should occur promptly, particularly if the hip or shoulder is involved. Diagnostic joint aspiration should be performed as soon as possible so that surgical drainage (if necessary) and appropriate empiric antimicrobial therapy can be instituted. Early diagnosis and treatment is associated with improved outcome. It is difficult to provide a threshold for the "critical window" of time for joint drainage and initiation of antibiotics. However, case series consistently suggest that joint injury is more likely when joint drainage and initiation of antibiotics are performed four or more days after the onset of symptoms, particularly in children with septic arthritis of the hip. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Outcome'.)

The goals of the evaluation are to confirm the presence of bacteria in the joint and to exclude other conditions in the differential diagnosis. (See 'Differential diagnosis' below.)

History — Important aspects of the history in the child with suspected infectious arthritis include (table 2) [3,25] (see "Bacterial arthritis: Epidemiology, pathogenesis, and microbiology in infants and children", section on 'Microbiology'):

Progression of symptoms – The pain of untreated bacterial arthritis tends to worsen over time; it does not wax and wane. The pain may awaken the patient at night, in contrast to the pain of inflammatory arthropathies such as juvenile idiopathic arthritis, in which symptoms tend to be worst upon rising in the morning. Complaints of knee or thigh pain may represent referred pain from pathology in the hip (bacterial arthritis or other hip pathology).

Joint trauma – Joint trauma may provide an entry point for direct inoculation (eg, animal bites, kneeling on needles, puncture wounds [eg, from broken glass] or lacerations over a joint), which may be associated with unusual pathogens (eg, Pasteurella, anaerobes, Sporothrix schenckii), in contrast to the typical pathogens that usually enter the joint from the bloodstream.

Skin lesions – Skin lesions may occur in bacterial arthritis due to N. gonorrhoeae (picture 2) or N. meningitidis (picture 3) [26]. Skin lesions also may provide a clue to several considerations in the differential diagnosis (table 3 and table 4). (See 'Differential diagnosis' below.)

Skin and soft tissue infections (eg, impetigo, cellulitis, abscess) may provide a portal of entry for S. aureus or group A streptococci (Streptococcus pyogenes), leading to bacteremia.

Recent use of antibiotics – The recent use of antibiotics may attenuate symptoms. It also may provide a clue to an antecedent infection that may be associated with postinfectious arthritis (eg, poststreptococcal reactive arthritis) or predispose to infection with a resistant pathogen (eg, penicillin-resistant pneumococcus) [27]. Serum sickness-like reactions also may follow exposure to many antibiotics, including penicillins, cephalosporins, ciprofloxacin, and sulfonamides. (See "Serum sickness and serum sickness-like reactions", section on 'Serum sickness-like reactions'.)

Recent or concurrent illness – Upper respiratory tract infection may precede bacterial arthritis (predisposing to bacteremia) or may precede or possibly represent a viral cause of transient synovitis (also called toxic synovitis). Enteric, genitourinary, and respiratory infections may precede postinfectious reactive arthritis. Concurrent varicella-zoster virus (VZV) infection may provide a portal of entry for S. aureus or group A streptococcal bacteremia; VZV itself also can rarely cause arthritis. (See "Bacterial arthritis: Epidemiology, pathogenesis, and microbiology in infants and children", section on 'Pathogenesis' and 'Differential diagnosis' below.)

History of sickle cell disease – Patients with sickle cell disease may have vaso-occlusive joint pain and/or may develop bacterial arthritis as a complication of sickle cell disease [28]. (See "Acute and chronic bone complications of sickle cell disease", section on 'Osteomyelitis and septic arthritis'.)

Onset of most recent menses (for pubertal females) – Disseminated gonococcal infection usually occurs in the first seven days of the menstrual cycle [29]. (See "Disseminated gonococcal infection", section on 'Clinical manifestations'.)

Exposures – Reviewing the history (including recent travel) for various exposures may suggest particular pathogens or other conditions (eg, hepatitis B, Lyme disease, Mycobacterium tuberculosis, coccidioidomycosis, histoplasmosis, chikungunya virus). (See "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents", section on 'Epidemiology' and "Epidemiology of Lyme disease" and "Primary pulmonary coccidioidal infection", section on 'Epidemiology' and "Pathogenesis and clinical features of pulmonary histoplasmosis", section on 'Reservoir' and "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Epidemiology'.)

Immunization status – Arthritis due to Haemophilus influenzae type b, Streptococcus pneumoniae, hepatitis B virus, measles, and mumps may occur in unimmunized children. However, in the post-pneumococcal conjugate vaccine era, most cases of S. pneumoniae arthritis are caused by nonvaccine serotypes (particularly 35B and 33F) [30]. Receipt of rubella vaccine virus is associated with joint symptoms two weeks after immunization.

Family history of rheumatologic disease (eg, psoriatic arthritis) or inflammatory bowel disease may suggest an alternative cause for the joint complaints.

Physical examination — Physical examination may confirm the presence and location of acute arthritis and may identify a source of bacteremia or entry point for direct inoculation. Examination also may provide support for conditions in the differential diagnosis (table 3 and table 4). (See 'Differential diagnosis' below.)

Observation – Observation is an important aspect of the physical examination of the infant or child with suspected bacterial arthritis [25]. Infants and children with bacterial arthritis usually appear ill and may have overt signs of sepsis (eg, tachycardia, tachypnea, hypotension, pallor). They tend to maintain the joint in a position that maximizes comfort. Knees are held moderately flexed. Hips are flexed, abducted, and externally rotated in an attempt to maintain the position causing the least pain from stretching the joint capsule. Position preference to maximize comfort is a nonspecific finding; it may occur in any condition with increased intra-articular fluid (eg, hemarthrosis from hemophilia, sterile effusion) [22,31]. Children with bacterial arthritis may refuse to bear weight on or use the involved extremity.

Skin examination – Skin lesions may occur in bacterial arthritis due to N. gonorrhoeae (picture 2) or N. meningitidis (picture 3) [26]. Rash also may provide a clue to several considerations in the differential diagnosis (eg, Lyme disease (picture 4A-B), juvenile idiopathic arthritis (picture 5), VZV (picture 6), enteroviral infections, serum sickness-like reaction). (See 'Differential diagnosis' below.)

Eye examination – Examination of the eyes may help to identify other causes of arthritis in children (eg, nonexudative conjunctivitis in Kawasaki disease, conjunctivitis or uveitis in reactive arthritis or juvenile idiopathic arthritis). (See 'Differential diagnosis' below.)

Liver examination – Hepatomegaly may be a clue to brucella arthritis in a child with foreign travel or other potential exposure to brucellosis (eg, consuming unpasteurized dairy products). In a retrospective case series of 133 children with osteoarticular brucellosis, 74 percent had associated hepatomegaly. In smaller case series, the frequency of hepatomegaly ranged from 17 to 44 percent [32]. (See "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Musculoskeletal examination – All bones should be palpated and all joints moved; the area(s) of suspected involvement should be examined last. Finding several abnormal joints makes bacterial arthritis less likely than viral, reactive, or inflammatory arthropathies, which are more commonly polyarticular. If the child is frightened or uncooperative, the parent/caregiver can be instructed to perform the joint examination while the clinician observes from a distance.

The involved joint is typically swollen, red, warm, and tender to palpation (picture 1A-B). External findings may be absent when the hip is involved, although asymmetric buttock creases or swelling of a buttock or the genitalia may provide a clue [33]. Severe swelling may indicate extensive infection or venous thrombosis (sometimes associated with S. aureus osteoarticular infections) [17,34]. Changes in the adjacent soft tissue are variable and depend upon the duration of infection and the depth of the joint [35,36]. Subtle soft tissue findings may include loss of normal concavity and skin markings [25].

Active and passive range of motion usually are decreased. Pain through any range of active or passive motion is suggestive of bacterial arthritis. In contrast, children with traumatic injuries and other types of arthritis usually have some pain-free range of motion [25]. Pain is increased with maneuvers that increase intracapsular pressure (eg, compression of the head of the femur into the acetabulum in patients with bacterial arthritis of the hip). In patients with bacterial arthritis of the sacroiliac joint, maneuvers that twist the pelvis cause pain (eg, the FABERE test (figure 1)), whereas gentle hip motion does not [22,23,37].

Laboratory evaluation — The laboratory evaluation for children with suspected bacterial arthritis typically includes [25,38-40]:

Complete blood count with differential

C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR)

Blood culture

Synovial fluid analysis (white blood cell [WBC] count and differential, Gram stain, culture, susceptibility testing, and polymerase chain [PCR] assay for Kingella for children under 36 months of age, if available)

Additional laboratory studies may be necessary in patients in whom particular organisms are suspected (eg, N. gonorrhoeae, group A Streptococcus). (See 'Other studies' below.)

When appropriate cultures and other studies are obtained (synovial fluid, blood, and other sites as indicated), the bacterial etiology is confirmed in 30 to 50 percent of cases [41,42].

Blood tests — The peripheral WBC count, CRP, and/or ESR are usually elevated in patients with bacterial arthritis. However, in some cases, they are only mildly elevated [6,43-45]. CRP and/or ESR are better negative than positive predictors of bacterial arthritis [46]. When elevated, they can be used to monitor the disease course and response to treatment. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Response to therapy'.)

The CRP is elevated in most patients with bacterial arthritis [47-49]. In one study of 100 children with bacterial arthritis, the mean CRP was 8.5 mg/dL (85 mg/L) [47]. The CRP tend to be higher in children with concomitant osteomyelitis or extensive soft tissue involvement compared with children with isolated bacterial arthritis [50-53].

Normal CRP is a good negative predictor for bacterial arthritis. In a retrospective series of 133 children who underwent joint aspiration and in whom CRP was obtained, 39 children (29 percent) had bacterial arthritis. A CRP <1 mg/dL (10 mg/L) was associated with a negative predictive value of 87 percent for positive synovial fluid culture [46]. CRP is more useful than ESR for monitoring response to treatment [46,47,54]; the CRP peaks within 36 to 50 hours of onset of infection and usually falls to normal within a week of successful treatment, whereas ESR may remain elevated for up to 30 days [25,47].

By contrast, the ESR is >20 mm/hour in most children with bacterial arthritis (mean 55 mm/hour) [6,36,43,47,55]. The ESR may rise for three to five days after institution of appropriate therapy [47]; continuing to rise after three to five days may be an indication of treatment failure [25]. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Response to therapy'.)

We recommend that aerobic blood cultures be obtained in all patients in whom bacterial arthritis is a consideration. Blood cultures are positive in as many as 40 percent of cases and sometimes yield the pathogen when joint fluid cultures are negative [9,25,30,50,51,56]. Anaerobic cultures should be obtained if anaerobic infection is a concern (eg, direct inoculation or in jugular vein suppurative thrombophlebitis [also known as Lemierre syndrome], which is typically caused by Fusobacterium infection [57,58]). (See "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein".)

Serology for antibody to Borrelia antigens should be sent when Lyme disease-related articular disease is suspected based upon the geographic location, or the possibility of exposure to vectors of Lyme disease [59]. Physical examination findings and laboratory tests alone cannot distinguish Lyme arthritis from acute bacterial arthritis caused by routine pathogens [59-61]. (See "Diagnosis of Lyme disease" and "Musculoskeletal manifestations of Lyme disease", section on 'Late Lyme disease'.)

Synovial fluid — Aspiration of synovial fluid should be performed as soon as possible when bacterial arthritis is suspected [25,62]. The identification of organisms in synovial fluid is the primary criterion for the diagnosis of bacterial arthritis. In addition, removal of synovial fluid decompresses the joint, which makes the patient more comfortable and is an essential component of treatment. (See 'Diagnosis' below.)

Early diagnosis and treatment is associated with improved outcome. It is difficult to provide a threshold for the "critical window" of time for joint drainage and initiation of antibiotics. However, case series consistently suggest that joint injury is more likely when joint drainage and initiation of antibiotics are performed four or more days after the onset of symptoms, particularly in children with septic arthritis of the hip. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Outcome'.)

Joint aspiration in children is discussed separately. (See "Joint aspiration or injection in children: Indications, technique, and complications".)

The following are important aspects of ensuring the collection of an appropriate specimen:

Hip aspiration should be performed with ultrasound guidance to confirm joint entry.

Magnetic resonance imaging (MRI) before aspiration of any joint may be warranted in children at increased risk of adjacent bone or soft tissue infection [10,11]. Adjacent infections may require surgical drainage or debridement, or increased duration of antimicrobial therapy, and may identify additional sites for culture. However, MRI usually requires sedation in small children and may introduce an unacceptable delay in management of septic arthritis of the hip and shoulder. (See 'Other imaging tests' below.)

Synovial fluid should be collected in a heparinized syringe so that clot formation does not preclude enumeration of leukocytes.

Synovial fluid should be sent for cell count, Gram stain, culture (aerobic and anaerobic), susceptibility testing, and PCR assay for Kingella in children under 36 months of age (if available). For children between 1 and 36 months of age, joint fluid should be injected into blood culture bottles to enhance the recovery of Kingella kingae (usually seen in children <36 months of age). PCR testing of synovial fluid for K. kingae and other fastidious pathogens increases detection, particularly in patients who received antibiotics before synovial fluid sampling [63-68]. PCR for S. aureus, group A Streptococcus, and S. pneumoniae is also available in some reference laboratories.

Additional studies and/or special culture media may be necessary if less common organisms are suspected (eg, fungi and acid fast bacilli).

Synovial fluid interpretation

Cell count – The synovial fluid WBC count must be used in conjunction with clinical findings when making decisions regarding treatment of arthritis while awaiting results of the Gram stain and culture [69,70]. (See 'Diagnosis' below and "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Empiric parenteral therapy'.)

The higher the synovial fluid WBC count, the greater the likelihood of bacterial arthritis [71,72]. Synovial fluid WBC counts of >50,000 cells/microL, with a predominance (>90 percent) of polymorphonuclear leukocytes, suggest bacterial arthritis [38,62,73-75]. However, a synovial fluid WBC count of >50,000 is neither sensitive nor specific for bacterial arthritis [7,69,71,72]. The synovial fluid WBC count may be <50,000 cells/microL in patients with unusual causes of bacterial arthritis (eg, Brucella) and may exceed 50,000 cells/microL in children with juvenile idiopathic arthritis, serum sickness, or reactive arthritis [70,71,76].

Gram stain – The importance of careful examination of the Gram-stained smear of synovial fluid cannot be overemphasized. Organisms that are seen on the Gram-stained smear may not grow in culture because synovial fluid has bacteriostatic effects. Approximately 40 to 50 percent of joint aspirates are sterile in patients with other clinical and laboratory findings of bacterial arthritis, including positive blood cultures [5,6,56,77,78]. On the other hand, positive findings on Gram stain are not definitive, as cellular debris may be misinterpreted as bacteria.

Culture – The identification of organisms in joint fluid is the primary criterion for the diagnosis of bacterial arthritis. Synovial fluid should be cultured under aerobic and anaerobic conditions. For children between 1 and 36 months of age, joint fluid should be injected into blood culture bottles to enhance the recovery of K. kingae.

Synovial fluid cultures are positive in as many as 50 to 60 percent of patients with other clinical and laboratory findings of bacterial arthritis [5,6,50,51,56,77,78]. False negative synovial fluid cultures may occur with fastidious organisms (eg, K. kingae, N. gonorrhoeae), inadequate laboratory techniques, or prior treatment with antibiotics [42]. The use of cell lysis (blood culture) bottles and incubation for at least seven days may enhance the recovery of K. kingae and other organisms [79,80].

Polymerase chain reaction (PCR) – PCR testing of synovial fluid for K. kingae (generally seen in children <36 months of age) and other fastidious pathogens increases detection, particularly in patients who received antibiotics before synovial fluid sampling [63-66]. PCR for S. aureus, group A Streptococcus, and S. pneumoniae is also available in some reference laboratories.

Culture for unusual pathogens – Synovial fluid should be cultured for unusual pathogens in patients with:

History of tuberculosis exposure (M. tuberculosis) (see "Bone and joint tuberculosis")

History of trauma, animal bite or scratch, or a mechanism for direct inoculation (anaerobes, Pasteurella, sporotrichosis) (see "Pasteurella infections" and "Clinical features and diagnosis of sporotrichosis")

Travel to or living in an area endemic for fungal infections (eg, coccidioidomycosis) or brucellosis (see "Primary pulmonary coccidioidal infection", section on 'Epidemiology' and "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis")

Immune suppression (candidal arthritis)

Monoarthritis that is refractory to initial antibacterial therapy (Brucella, tuberculosis) (see "Bone and joint tuberculosis" and "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis")

Other studies — Additional laboratory studies may be necessary in patients in whom particular organisms are suspected (table 1):

If gonococcal arthritis is suspected in adolescent patients, nucleic acid testing or cultures from the oropharynx, rectum, cervix (females) or urethra (males), and skin lesions (if present) are indicated. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Diagnostic approach'.)

If gonococcal infection is suspected in the newborn, culture of the cerebrospinal fluid should be obtained in addition to cultures of blood and eye exudates. (See "Gonococcal infection in the newborn".)

If group A streptococcal arthritis, poststreptococcal arthritis, or rheumatic fever is suspected, throat culture and/or antistreptolysin-O (ASO) titer should be obtained. (See "Acute rheumatic fever: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

Cultures of the stool and/or urine should be obtained if septic arthritis due to gram-negative enteric pathogens or reactive arthritis following gastrointestinal tract infection is suspected. (See "Bacterial arthritis: Epidemiology, pathogenesis, and microbiology in infants and children", section on 'Microbiology'.)

Serology for coccidioidomycosis should be considered for patients who live in the endemic area, principally the western United States and parts of Mexico [81]. (See "Primary pulmonary coccidioidal infection", section on 'Epidemiology'.)

Imaging

Goals and approach — Imaging is an important adjunct to the physical examination of the child with suspected bacterial arthritis. Imaging can confirm joint effusion in joints that are difficult to examine (eg, hip, shoulder, sacroiliac joint). However, joint effusion is not specific for bacterial arthritis.

Imaging is also helpful in identifying concomitant osteomyelitis and evaluating other conditions in the differential diagnosis (eg, trauma, osteomyelitis without concomitant bacterial arthritis) [44,82,83]. (See 'Diagnosis' below and 'Differential diagnosis' below.)

The radiologic evaluation usually begins with radiographs to identify fractures, foci of osteomyelitis, and other causes of osteoarticular pain and swelling. They can also identify radio-opaque foreign bodies. Although radiographs may demonstrate signs of capsular swelling, they are not particularly sensitive in detecting joint effusion [44,84,85]. Ultrasonography and MRI are sensitive in detecting joint effusion, but ultrasonography is more widely and readily available, less costly, and does not require sedation in young children.

Other imaging tests may be necessary in specific circumstances (eg, additional evaluation for concomitant osteomyelitis, evaluation of deep joints or complex anatomy, failure to respond to initial management).

Radiographs

Radiographic findings – The radiographic findings of bacterial arthritis are related to capsular swelling. Radiographs add little to the diagnostic evaluation of joints that are readily accessible to physical examination but may be a valuable adjunct to the examination of the hip.

When reviewing radiographs, it is helpful to compare the involved extremity with the opposite side [33]. Radiographic findings suggestive of joint effusion and/or bacterial arthritis include [9,15,33,50,85,86]:

Soft tissue swelling

Displacement of muscle surrounding the joint

Widening of the joint space

Increased opacity within the joint

Distension of the joint capsule

Subluxation

Erosion or disappearance of the epiphysis or metaphysis (present two to four weeks after the onset), suggesting adjacent osteomyelitis

Erosion of subchondral bone (present two to four weeks after the onset)

In a retrospective cohort of 28 children with bacterial arthritis without concomitant osteomyelitis who underwent imaging with radiography, 13 had joint effusion and synovial swelling, 2 had bone and periosteal changes, and 5 had skin and soft tissue changes [50].

Findings on hip radiographs – Hip radiographs may demonstrate findings suggestive of bacterial arthritis and are necessary to exclude other conditions that cause hip pain (eg, Legg-Calvé-Perthes disease, slipped capital femoral epiphysis, fracture) [87]. (See "Approach to hip pain in childhood", section on 'Common causes of hip pain in children'.)

In the child with suspected bacterial arthritis of the hip, radiographs should be obtained with the child in the "frog leg position" and with the legs extended at the knee and slightly internally rotated. It is better to request an anteroposterior and frog lateral radiograph of the pelvis than views of a single hip. Subtle changes (described below) may be more apparent when the opposite hip is readily visible on the same image.

Radiographic signs of hip arthritis may include [4,9,31,86,88-90]:

Swelling of the capsule

Obliteration or lateral displacement of the gluteal fat lines (image 1)

Elevation of the femoral portion of Shenton line, with widening of the arc

The obturator sign (the margins of the obturator internus are displaced medially into the pelvis as its tendon passes over the capsule of the hip joint)

Lateral and superior displacement of the femoral head with relatively normal acetabular development (in contrast to developmental dysplasia of the hip, in which the acetabulum is abnormal)

Concomitant osteomyelitis of the femur (this is a late sign, since bone demineralization or destruction takes a minimum of a week to become apparent on routine radiographs)

Ultrasonography — Ultrasonography is helpful in identifying and quantifying joint effusions, particularly for deep joints such as the hip (image 2) [39,44,87,91]. Ultrasonography has a high negative predictive value and can be used to guide diagnostic aspiration.

In a retrospective cohort of 34 children with bacterial arthritis without osteomyelitis who underwent imaging with ultrasonography, 31 (91 percent) had joint effusion and synovial swelling, 1 had bone and periosteal change, and 2 had skin and soft tissue changes [50].

In a series of 96 children who underwent hip ultrasonography for possible bacterial arthritis, none of the 40 who had normal sonographic findings had a discharge diagnosis of bacterial arthritis [44]. However, false negative ultrasonography has been reported when imaging was inadequate or performed less than 24 hours after the onset of symptoms [92].

Neither the presence of an effusion nor the sonographic characteristics of the fluid (ie, echolucent versus echogenic) correlate with the presence of infection [44,82,83]. Increased blood flow with power or color Doppler suggests infection, but normal blood flow does not exclude septic arthritis [93]. Consequently, if ultrasonography demonstrates fluid in the joint, diagnostic aspiration should be performed. (See 'Synovial fluid' above and "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Drainage'.)

Ultrasonographic guidance is recommended for diagnostic aspiration of the hip [94,95]. By contrast, imaging guidance is not always necessary for aspiration of other joints. However, if guidance is required for children younger than eight years, ultrasonography is preferred to fluoroscopy because ultrasonography demonstrates cartilaginous structures [94]. (See "Joint aspiration or injection in children: Indications, technique, and complications".)

Other imaging tests

MRI – MRI is highly sensitive for the early detection of joint fluid (image 3) [39,84]. However, it is not as readily available as ultrasonography, is more costly than ultrasonography, and may require sedation for younger children.

Changes in signal intensity of bone marrow are demonstrated more frequently in patients with bacterial arthritis of the hip than with transient synovitis and may be helpful in differentiating these conditions [84,96].

MRI also may demonstrate abnormalities of adjacent bone and soft tissues, as well as the extent of cartilage destruction. Children with concomitant osteomyelitis or extensive soft tissue involvement generally have a higher CRP or ESR at the time of presentation [52,53,97].

Bone scan – Radionuclide bone scans generally are not used in the diagnostic evaluation of bacterial arthritis unless concomitant osteomyelitis is suspected. MRI is preferred over a bone scan because it provides greater anatomic detail without radiation exposure. However, bone scans may be helpful in the evaluation of deep joints (eg, hip, sacroiliac) [9,22,24].

The characteristic bone scan finding in bacterial arthritis is increased uptake on both sides of the joint during the early or "blood pool" phase [98]. In contrast, in osteomyelitis, the bone scan generally demonstrates increased uptake on only one side of a joint.

Performance of radionuclide bone scan in patients in whom concomitant osteomyelitis is suspected should not delay aspiration of the joint or prompt surgical drainage when bacterial arthritis is suspected [87]. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Drainage'.)

Computed tomography – Although not routinely performed in the evaluation of suspected bacterial arthritis [99], computed tomography (CT) may be helpful in assessing areas of complex anatomy (eg, shoulder, hip, sacroiliac joint) [37]. In the later stages of the disease process, CT may demonstrate destructive changes [100].

DIAGNOSIS

Clinical suspicion – Acute bacterial arthritis should be suspected in children who present with fever and monoarticular pain, swelling, and limited range of motion and in young infants who present with clinical manifestations of sepsis (eg, irritability, poor feeding), pseudoparalysis, evidence of discomfort when handled or having the diaper changed, or fever without a focus.

In children with underlying juvenile idiopathic arthritis, bacterial arthritis should be suspected if there is unusual worsening of one joint during an exacerbation of arthritis or recent injection of the joint in question. (See 'Clinical features' above.)

Laboratory confirmation of bacterial arthritis – Isolation or identification of a bacterial pathogen from the synovial fluid (by Gram stain, culture, or other diagnostic technique) confirms the diagnosis of bacterial arthritis. Isolation of bacteria from blood cultures in a patient with characteristic clinical features (eg, fever and joint pain in an older child; clinical manifestations of sepsis or joint involvement in young infants) and increased synovial fluid white blood cell (WBC) count also confirms the diagnosis, even if the synovial fluid culture remains negative. When appropriate cultures are obtained (including cultures of blood and other sites as indicated), the bacterial etiology is confirmed in 50 to 70 percent of cases [5,6,77,78]. (See 'Synovial fluid' above and 'Blood tests' above.)

Probable bacterial arthritis (culture-negative arthritis) – A diagnosis of probable bacterial arthritis (or culture-negative arthritis) can be made in the absence of isolation of bacteria from synovial fluid or blood if other pathologic processes are excluded and the patient has characteristic clinical, laboratory, and radiographic findings [25,101,102]:

Clinical findings – Fever and joint pain in an older child; clinical manifestations of sepsis or joint involvement in young infants (see 'Clinical features' above)

Laboratory findings – Elevated synovial fluid WBC count (usually >50,000 cells/microL) with a predominance (usually >90 percent) of polymorphonuclear leukocytes (see 'Laboratory evaluation' above)

Radiographic findings – Evidence of joint effusion (see 'Imaging' above)

Consultation with an expert in pediatric infectious diseases and/or pediatric rheumatology may be helpful in difficult cases. (See 'Clinical features' above and 'Laboratory evaluation' above and 'Imaging' above.)

Given the potential morbidity of delayed treatment, children with probable bacterial arthritis should be managed in the same manner as children in whom infection has been confirmed by isolation of an organism from synovial fluid [102]. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Negative cultures'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of bacterial arthritis in infants and children includes other types of infectious and noninfectious arthritis (table 3 and table 4), other infections (musculoskeletal and systemic), and other causes of joint pain. Clinical features, imaging studies, and/or synovial fluid analysis usually differentiate these conditions from acute bacterial arthritis. Consultation with an expert in pediatric infectious diseases or pediatric rheumatology may be helpful in difficult cases. (See 'Indications for consultation' below.)

Other types of arthritis — Arthritis can be caused by viruses, mycobacteria, and fungi, as well as bacteria (table 3). Viral arthritis may be associated with other characteristic findings, such as rash (eg, varicella (picture 6), parvovirus (picture 7A-B), rubella (picture 8)) or parotitis (during the course of mumps) (picture 9). Viral arthritis may be polyarticular or monoarticular, and it may affect virtually any joint. Synovitis due to viral infections is typically characterized by pain and swelling, but not warmth or erythema, of multiple small joints, usually in the fingers.

Fungal arthritis is rare in children but can occur in neonates hospitalized in the intensive care unit, immunocompromised hosts, and in patients with coccidioidomycosis and other endemic mycoses. Fungal arthritis caused by opportunistic pathogens usually presents after an indolent course. (See "Clinical manifestations and diagnosis of Candida infection in neonates", section on 'Other focal infections' and "Viral arthritis: Causes and approach to evaluation and management".)

Postinfectious or reactive arthritis is associated with a recent or concomitant extra-articular infection of the upper respiratory (eg, H. influenzae, N. meningitidis, group A Streptococcus), gastrointestinal (Shigella, Salmonella, Campylobacter), or genitourinary tracts (Chlamydia trachomatis) [103-105]. (See "Reactive arthritis".)

Noninfectious causes of arthritis in children include trauma (hemarthrosis) and inflammatory and immunologic disorders. Associated clinical features usually help to differentiate these conditions from bacterial arthritis (table 4).

Other infections — Other musculoskeletal and systemic infections may have signs and symptoms that mimic those of bacterial arthritis (eg, fever, musculoskeletal pain, refusal to bear weight, joint swelling). These include:

Osteomyelitis – In children with osteomyelitis without concomitant bacterial arthritis, gentle examination usually allows some joint movement and pain-free range of motion, whereas in children with bacterial arthritis, there is pain through any range of active or passive motion [25,33,101]. (See "Hematogenous osteomyelitis in children: Clinical features and complications", section on 'Clinical features'.)

Deep cellulitis – Imaging studies may be necessary to exclude joint involvement in patients with deep cellulitis.

Obturator internus or psoas muscle abscess – Imaging studies may be necessary to differentiate obturator internus or psoas abscess from bacterial arthritis of the hip [106,107]. (See "Psoas abscess", section on 'Diagnosis'.)

Septic (suppurative) bursitis – Physical examination demonstrating peribursal erythema and warmth and aspiration of bursal fluid help to differentiate septic bursitis from bacterial arthritis [95,108]. (See "Septic bursitis".)

Bacterial endocarditis – Patients with bacterial endocarditis may have a systemic immune reaction that includes arthritis. The classic clinical stigmata of bacterial endocarditis, although uncommon in children, include petechiae, splinter hemorrhages (picture 10), Janeway lesions (picture 11), Osler nodes (picture 12), and Roth spots (exudative, edematous hemorrhagic lesions of the retina). (See "Infective endocarditis in children", section on 'Clinical manifestations'.)

Other causes of joint pain — Other causes of joint pain, limp, or refusal to bear weight in children are listed below. With the exception of malignant tumors, these conditions usually are not accompanied by fever or constitutional signs. They are discussed separately.

Transient (or toxic) synovitis (see "Approach to hip pain in childhood", section on 'Transient synovitis')

Trauma (eg, fracture)

Vaso-occlusive pain in children with sickle cell disease (see "Acute and chronic bone complications of sickle cell disease", section on 'Causes of bone or joint pain')

Slipped capital femoral epiphysis (see "Evaluation and management of slipped capital femoral epiphysis (SCFE)")

Legg-Calvé-Perthes disease (see "Approach to hip pain in childhood", section on 'Legg-Calvé-Perthes and secondary avascular necrosis')

Tumor (eg, leukemia, osteosarcoma, osteoid osteoma) (see "Overview of the clinical presentation and diagnosis of acute lymphoblastic leukemia/lymphoma in children", section on 'Presentation' and "Osteosarcoma: Epidemiology, pathology, clinical presentation, and diagnosis", section on 'Diagnostic evaluation' and "Nonmalignant bone lesions in children and adolescents", section on 'Osteoid osteoma')

Villonodular synovitis (a rare benign but locally invasive proliferative lesion of synovial tissue that limits joint function and may destroy adjacent bone) (see "Treatment for tenosynovial giant cell tumor and other benign neoplasms affecting soft tissue and bone", section on 'Tenosynovial giant cell tumor')

INDICATIONS FOR CONSULTATION — In the evaluation of the child with suspected bacterial arthritis, consultation with an expert in infectious diseases may be warranted for children with postoperative infection, chronic joint infection, perforating injury, or suspected unusual pathogens [94].

Consultation with an expert in rheumatology may be warranted for children with underlying arthritis (eg, juvenile idiopathic arthritis, psoriatic arthritis), involvement of more than one joint, or failure to respond to antibiotics. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Response to therapy'.)

Urgent consultation with an orthopedic surgeon generally is warranted in cases of suspected septic arthritis of the hip and shoulder, for which prompt drainage is recommended. Orthopedic consultation also may be warranted for irrigation and drainage of other joints. (See "Bacterial arthritis: Treatment and outcome in infants and children", section on 'Drainage'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Septic arthritis and osteomyelitis in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword[s] of interest.)

Basics topic (see "Patient education: Septic arthritis (The Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical features – Bacterial arthritis usually affects the lower extremity, predominantly the hip and knee. Up to 10 percent of cases involve more than one joint, particularly in neonates. The presentation of bacterial arthritis in infants and children varies depending upon the age of the child, the site of infection, and the causative organism (table 1). (See 'Clinical features' above.)

In neonates and young infants, the typical presentation is that of septicemia (eg, irritability, poor feeding), cellulitis, or fever without a focus of infection. Clues to joint involvement include lack of use of the involved extremity, aversion to or discomfort on being handled (eg, being picked up, having the diaper changed), postural changes (eg, positional preferences), and unilateral swelling of the extremity, buttocks, or genitalia. (See 'Neonates and infants' above.)

Older children generally have fever and constitutional symptoms in addition to swelling, tenderness, and limited mobility of the affected joint, but the joint findings may be subtle. (See 'Older children and adolescents' above.)

Timing and goals of evaluation – Evaluate infants and children with suspected bacterial arthritis promptly, particularly if the hip or shoulder is involved. Early diagnosis and treatment is associated with improved outcome. (See 'Timing and goals' above.)

History – Important aspects of the history in the child with suspected infectious arthritis are described in the table (table 2). (See 'History' above.)

Physical examination – Important aspects of the physical examination include (see 'Physical examination' above):

Observation of the child for restricted extremity use, a preferential position, and/or joint swelling and erythema (picture 1A-B)

Palpation of all bones and joints

Assessment of range of motion of all joints

Examination of the skin and eyes

Search for another focus of infection or source for bacteremia

Laboratory evaluation

Routine evaluation – The routine laboratory evaluation for children with suspected bacterial arthritis typically includes:

-Complete blood count with differential, C-reactive protein (CRP), and/or erythrocyte sedimentation rate (ESR)

The peripheral white blood cell (WBC) count, CRP, and ESR are usually elevated in patients with bacterial arthritis, but they are better negative than positive predictors of bacterial arthritis.

-Blood culture

-Synovial fluid WBC count, Gram stain, culture, and susceptibility testing

Synovial fluid WBC count of >50,000 cells/microL with >90 percent neutrophils is suggestive of bacterial arthritis, but the identification of organisms in the joint fluid is the primary criterion for diagnosis. (See 'Synovial fluid' above.)

Additional studies for select patients – Additional laboratory studies may be necessary in patients in whom particular organisms are suspected (table 1). (See 'Laboratory evaluation' above.)

Imaging – The radiologic evaluation of children with suspected bacterial arthritis usually begins with radiographs to identify fractures, foci of osteomyelitis, and other causes of osteoarticular pain and swelling.

Ultrasonography is helpful in detecting joint fluid, but the presence of fluid is not specific for joint infection. Magnetic resonance imaging is the most sensitive for the early detection of joint fluid and concomitant osteomyelitis but is not as readily available as ultrasonography and may require sedation for younger children. (See 'Imaging' above.)

Diagnosis

Confirmed – The diagnosis of bacterial arthritis is confirmed by (see 'Diagnosis' above):

-Isolation or identification of a bacterial pathogen from the synovial fluid (by culture, Gram stain, or other diagnostic technique, such as polymerase chain reaction), or

-Isolation of bacteria from blood cultures in a patient with characteristic clinical features (eg, fever and joint pain in an older child; clinical manifestations of sepsis, cellulitis, joint involvement, or fever without a focus in young infants) and increased synovial fluid WBC count (even if the synovial fluid culture remains negative)

Probable bacterial arthritis (culture-negative arthritis) – A diagnosis of probable bacterial arthritis (or culture-negative arthritis) that requires antimicrobial therapy can be made without isolation of bacteria from synovial fluid or blood if:

-Other pathologic processes are excluded, and the patient has:

-Characteristic clinical features (eg, fever and joint pain in an older child; clinical manifestations of sepsis, cellulitis, joint involvement, or fever without a focus in young infants), and

-Elevated synovial fluid WBC count with a predominance of polymorphonuclear leukocytes, and

-Evidence of joint effusion

Differential diagnosis – The differential diagnosis of bacterial arthritis includes other types of infectious and noninfectious arthritis (table 3 and table 4), other infections (musculoskeletal and systemic), and other causes of joint pain. Clinical features, imaging studies, and/or synovial fluid analysis usually differentiate these conditions from acute bacterial arthritis. (See 'Differential diagnosis' above.)

  1. Nade S. Septic arthritis. Best Pract Res Clin Rheumatol 2003; 17:183.
  2. Krogstad P. Septic arthritis. In: Feigin and Cherry’s Textbook of Pediatric Infectious Diseases, 8th ed, Cherry JD, Harrison G, Kaplan SL, et al (Eds), Elsevier, Philadelphia 2018. p.529.
  3. Arnold JC, Bradley JS. Osteoarticular Infections in Children. Infect Dis Clin North Am 2015; 29:557.
  4. OBLETZ BE. Suppurative arthritis of the hip joint in infants. Clin Orthop 1962; 22:27.
  5. Nelson JD. The bacterial etiology and antibiotic management of septic arthritis in infants and children. Pediatrics 1972; 50:437.
  6. Welkon CJ, Long SS, Fisher MC, Alburger PD. Pyogenic arthritis in infants and children: a review of 95 cases. Pediatr Infect Dis 1986; 5:669.
  7. Fink CW, Nelson JD. Septic arthritis and osteomyelitis in children. Clin Rheum Dis 1986; 12:423.
  8. Dan M. Septic arthritis in young infants: clinical and microbiologic correlations and therapeutic implications. Rev Infect Dis 1984; 6:147.
  9. Hong DK, Gutierrez K. Infectious and inflammatory arthritis. In: Principles and Practice of Pediatric Infectious Diseases, 5th ed, Long SS, Prober CG, Fischer M (Eds), Elsevier, Philadelphia 2018. p.487.
  10. Siddiqui AA, Andras LM, Illingworth KD, Skaggs DL. Pain for Greater Than 4 Days Is Highly Predictive of Concomitant Osteomyelitis in Children With Septic Arthritis. J Pediatr Orthop 2021; 41:255.
  11. Rosenfeld S, Bernstein DT, Daram S, et al. Predicting the Presence of Adjacent Infections in Septic Arthritis in Children. J Pediatr Orthop 2016; 36:70.
  12. Chung SM, Pollis RE. Diagnostic pitfalls in septic arthritis of the hip in infants and children. Clin Pediatr (Phila) 1975; 14:758.
  13. OBLETZ BE. Acute suppurative arthritis of the hip in the neonatal period. J Bone Joint Surg Am 1960; 42-A:23.
  14. Yagupsky P, Bar-Ziv Y, Howard CB, Dagan R. Epidemiology, etiology, and clinical features of septic arthritis in children younger than 24 months. Arch Pediatr Adolesc Med 1995; 149:537.
  15. Omene JA, Odita JC. Clinical and radiological features of neonatal septic arthritis. Trop Geogr Med 1979; 31:207.
  16. Asnes RS, Arendar GM. Septic arthritis of the hip: a complication of femoral venipuncture. Pediatrics 1966; 38:837.
  17. Chacha PB. Suppurative arthritis of the hip joint in infancy. A persistent diagnostic problem and possible complication of femoral venipuncture. J Bone Joint Surg Am 1971; 53:538.
  18. Freiberg JA, Perlman R. Pelvic abscesses associated with acute purulent infection of the hip joint. J Bone Joint Surg 1936; 18:417.
  19. Gillespie R. Septic arthritis of childhood. Clin Orthop Relat Res 1973; :152.
  20. Fleisher G. Infectious disease emergencies. In: Textbook of Pediatric Emergency Medicine, 5th ed, Fleisher GR, Ludwig S, Henretig FM (Eds), Lippincott, Williams & Wilkins, Philadelphia 2006. p.783.
  21. Osman AA, Govender S. Septic sacroiliitis. Clin Orthop Relat Res 1995; :214.
  22. Schaad UB, McCracken GH Jr, Nelson JD. Pyogenic arthritis of the sacroiliac joint in pediatric patients. Pediatrics 1980; 66:375.
  23. Molinos Quintana A, Morillo Gutiérrez B, Camacho Lovillo MS, et al. Pyogenic sacroiliitis in children-a diagnostic challenge. Clin Rheumatol 2011; 30:107.
  24. Alcobendas RM, Loza SM, Camba AR, et al. Sacroilitis in Preschool Children: A Case Series and Review of the Literature. Pediatr Infect Dis J 2020; 39:e272.
  25. Stans AA. Musculoskeletal infection. In: Lovell and Winter’s Pediatric Orthopaedics, 7th ed, Weinstein SL, Flynn JM (Eds), Wolters Kluwer Health, Philadelphia 2014. p.369.
  26. Rompalo AM, Hook EW 3rd, Roberts PL, et al. The acute arthritis-dermatitis syndrome. The changing importance of Neisseria gonorrhoeae and Neisseria meningitidis. Arch Intern Med 1987; 147:281.
  27. Bradley JS, Kaplan SL, Tan TQ, et al. Pediatric pneumococcal bone and joint infections. The Pediatric Multicenter Pneumococcal Surveillance Study Group (PMPSSG). Pediatrics 1998; 102:1376.
  28. Kaplan J, Ikeda S, McNeil JC, et al. Microbiology of Osteoarticular Infections in Patients with Sickle Hemoglobinopathies at Texas Children's Hospital, 2000-2018. Pediatr Infect Dis J 2019; 38:1251.
  29. Holmes KK, Counts GW, Beaty HN. Disseminated gonococcal infection. Ann Intern Med 1971; 74:979.
  30. Olarte L, Romero J, Barson W, et al. Osteoarticular Infections Caused by Streptococcus pneumoniae in Children in the Post-Pneumococcal Conjugate Vaccine Era. Pediatr Infect Dis J 2017; 36:1201.
  31. Bennett OM, Namnyak SS. Acute septic arthritis of the hip joint in infancy and childhood. Clin Orthop Relat Res 1992; :123.
  32. Bosilkovski M, Kirova-Urosevic V, Cekovska Z, et al. Osteoarticular involvement in childhood brucellosis: experience with 133 cases in an endemic region. Pediatr Infect Dis J 2013; 32:815.
  33. Nade S. Acute septic arthritis in infancy and childhood. J Bone Joint Surg Br 1983; 65:234.
  34. Walsh S, Phillips F. Deep vein thrombosis associated with pediatric musculoskeletal sepsis. J Pediatr Orthop 2002; 22:329.
  35. Nelson JD. Skeletal infections in children. Adv Pediatr Infect Dis 1991; 6:59.
  36. Shaw BA, Kasser JR. Acute septic arthritis in infancy and childhood. Clin Orthop Relat Res 1990; :212.
  37. Aprin H, Turen C. Pyogenic sacroiliitis in children. Clin Orthop Relat Res 1993; :98.
  38. Shmerling RH, Delbanco TL, Tosteson AN, Trentham DE. Synovial fluid tests. What should be ordered? JAMA 1990; 264:1009.
  39. Saavedra-Lozano J, Falup-Pecurariu O, Faust SN, et al. Bone and Joint Infections. Pediatr Infect Dis J 2017; 36:788.
  40. Walinga AB, Stornebrink T, Langerhuizen DWG, et al. What are the best diagnostic tests for diagnosing bacterial arthritis of a native joint? : a systematic review of 27 studies. Bone Joint J 2021; 103-B:1745.
  41. Spyridakis E, Gerber JS, Schriver E, et al. Clinical Features and Outcomes of Children with Culture-Negative Septic Arthritis. J Pediatric Infect Dis Soc 2019; 8:228.
  42. Klosterman MM, Villani MC, Hamilton EC, et al. Primary Septic Arthritis in Children Demonstrates Presumed and Confirmed Varieties Which Require Age-specific Evaluation and Treatment Strategies. J Pediatr Orthop 2022; 42:e27.
  43. Del Beccaro MA, Champoux AN, Bockers T, Mendelman PM. Septic arthritis versus transient synovitis of the hip: the value of screening laboratory tests. Ann Emerg Med 1992; 21:1418.
  44. Zawin JK, Hoffer FA, Rand FF, Teele RL. Joint effusion in children with an irritable hip: US diagnosis and aspiration. Radiology 1993; 187:459.
  45. Klein DM, Barbera C, Gray ST, et al. Sensitivity of objective parameters in the diagnosis of pediatric septic hips. Clin Orthop Relat Res 1997; :153.
  46. Levine MJ, McGuire KJ, McGowan KL, Flynn JM. Assessment of the test characteristics of C-reactive protein for septic arthritis in children. J Pediatr Orthop 2003; 23:373.
  47. Kallio MJ, Unkila-Kallio L, Aalto K, Peltola H. Serum C-reactive protein, erythrocyte sedimentation rate and white blood cell count in septic arthritis of children. Pediatr Infect Dis J 1997; 16:411.
  48. Singhal R, Perry DC, Khan FN, et al. The use of CRP within a clinical prediction algorithm for the differentiation of septic arthritis and transient synovitis in children. J Bone Joint Surg Br 2011; 93:1556.
  49. Caird MS, Flynn JM, Leung YL, et al. Factors distinguishing septic arthritis from transient synovitis of the hip in children. A prospective study. J Bone Joint Surg Am 2006; 88:1251.
  50. Manz N, Krieg AH, Heininger U, Ritz N. Evaluation of the current use of imaging modalities and pathogen detection in children with acute osteomyelitis and septic arthritis. Eur J Pediatr 2018; 177:1071.
  51. Calvo C, Núñez E, Camacho M, et al. Epidemiology and Management of Acute, Uncomplicated Septic Arthritis and Osteomyelitis: Spanish Multicenter Study. Pediatr Infect Dis J 2016; 35:1288.
  52. Pääkkönen M, Kallio MJ, Kallio PE, Peltola H. Sensitivity of erythrocyte sedimentation rate and C-reactive protein in childhood bone and joint infections. Clin Orthop Relat Res 2010; 468:861.
  53. Roine I, Faingezicht I, Arguedas A, et al. Serial serum C-reactive protein to monitor recovery from acute hematogenous osteomyelitis in children. Pediatr Infect Dis J 1995; 14:40.
  54. Wall EJ. Childhood osteomyelitis and septic arthritis. Curr Opin Pediatr 1998; 10:73.
  55. Deanehan JK, Kimia AA, Tan Tanny SP, et al. Distinguishing Lyme from septic knee monoarthritis in Lyme disease-endemic areas. Pediatrics 2013; 131:e695.
  56. Nade S, Robertson FW, Taylor TK. Antibiotics in the treatment of acute osteomyelitis and acute septic arthritis in children. Med J Aust 1974; 2:703.
  57. Trapp CM, Tamai J, Schleiss MR. Septic arthritis secondary to fusobacterium necrophorum in a 4-year-old girl: case report and review of the literature. Pediatr Infect Dis J 2005; 24:846.
  58. Section J, Gibbons SD, Barton T, et al. Microbiological culture methods for pediatric musculoskeletal infection: a guideline for optimal use. J Bone Joint Surg Am 2015; 97:441.
  59. Thompson A, Mannix R, Bachur R. Acute pediatric monoarticular arthritis: distinguishing lyme arthritis from other etiologies. Pediatrics 2009; 123:959.
  60. Bachur RG, Adams CM, Monuteaux MC. Evaluating the child with acute hip pain ("irritable hip") in a Lyme endemic region. J Pediatr 2015; 166:407.
  61. Glotzbecker MP, Kocher MS, Sundel RP, et al. Primary lyme arthritis of the pediatric hip. J Pediatr Orthop 2011; 31:787.
  62. Kunnamo I, Pelkonen P. Routine analysis of synovial fluid cells is of value in the differential diagnosis of arthritis in children. J Rheumatol 1986; 13:1076.
  63. Rosey AL, Abachin E, Quesnes G, et al. Development of a broad-range 16S rDNA real-time PCR for the diagnosis of septic arthritis in children. J Microbiol Methods 2007; 68:88.
  64. Carter K, Doern C, Jo CH, Copley LA. The Clinical Usefulness of Polymerase Chain Reaction as a Supplemental Diagnostic Tool in the Evaluation and the Treatment of Children With Septic Arthritis. J Pediatr Orthop 2016; 36:167.
  65. Ferroni A, Al Khoury H, Dana C, et al. Prospective survey of acute osteoarticular infections in a French paediatric orthopedic surgery unit. Clin Microbiol Infect 2013; 19:822.
  66. Hashavya S, Gross I, Michael-Gayego A, et al. The efficacy of 16S ribosomal DNA sequencing in the diagnosis of bacteria from blood, bone and synovial fluid samples of children with musculoskeletal infections. J Child Orthop 2018; 12:204.
  67. Samara E, Spyropoulou V, Tabard-Fougère A, et al. Kingella kingae and Osteoarticular Infections. Pediatrics 2019; 144.
  68. Villani MC, Hamilton EC, Klosterman MM, et al. Primary Septic Arthritis Among Children 6 to 48 Months of Age: Implications for PCR Acquisition and Empiric Antimicrobial Selection. J Pediatr Orthop 2021; 41:190.
  69. Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA 2007; 297:1478.
  70. Baldassare AR, Chang F, Zuckner J. Markedly raised synovial fluid leucocyte counts not associated with infectious arthritis in children. Ann Rheum Dis 1978; 37:404.
  71. Coutlakis PJ, Roberts WN, Wise CM. Another look at synovial fluid leukocytosis and infection. J Clin Rheumatol 2002; 8:67.
  72. Dart AH, Michelson KA, Aronson PL, et al. Hip Synovial Fluid Cell Counts in Children From a Lyme Disease Endemic Area. Pediatrics 2018; 141.
  73. Ropes MW. Examination of synovial fluid. Bull Rheum Dis 1957; 7 Suppl:S21.
  74. WARD J, COHEN AS, BAUER W. The diagnosis and therapy of acute suppurative arthritis. Arthritis Rheum 1960; 3:522.
  75. Heyworth BE, Shore BJ, Donohue KS, et al. Management of pediatric patients with synovial fluid white blood-cell counts of 25,000 to 75,000 cells/mm³ after aspiration of the hip. J Bone Joint Surg Am 2015; 97:389.
  76. Press J, Peled N, Buskila D, Yagupsky P. Leukocyte count in the synovial fluid of children with culture-proven brucellar arthritis. Clin Rheumatol 2002; 21:191.
  77. Barton LL, Dunkle LM, Habib FH. Septic arthritis in childhood. A 13-year review. Am J Dis Child 1987; 141:898.
  78. Wiley JJ, Fraser GA. Septic arthritis in childhood. Can J Surg 1979; 22:326.
  79. Yagupsky P, Press J. Use of the isolator 1.5 microbial tube for culture of synovial fluid from patients with septic arthritis. J Clin Microbiol 1997; 35:2410.
  80. Kiang KM, Ogunmodede F, Juni BA, et al. Outbreak of osteomyelitis/septic arthritis caused by Kingella kingae among child care center attendees. Pediatrics 2005; 116:e206.
  81. Bayer AS, Guze LB. Fungal arthritis. II. Coccidioidal synovitis: clinical, diagnostic, therapeutic, and prognostic considerations. Semin Arthritis Rheum 1979; 8:200.
  82. Miralles M, Gonzalez G, Pulpeiro JR, et al. Sonography of the painful hip in children: 500 consecutive cases. AJR Am J Roentgenol 1989; 152:579.
  83. Robben SG, Lequin MH, Diepstraten AF, et al. Anterior joint capsule of the normal hip and in children with transient synovitis: US study with anatomic and histologic correlation. Radiology 1999; 210:499.
  84. Buchmann RF, Jaramillo D. Imaging of articular disorders in children. Radiol Clin North Am 2004; 42:151.
  85. Volberg FM, Sumner TE, Abramson JS, Winchester PH. Unreliability of radiographic diagnosis of septic hip in children. Pediatrics 1984; 74:118.
  86. Mitchell M, Howard B, Haller J, et al. Septic arthritis. Radiol Clin North Am 1988; 26:1295.
  87. Swami SK, Eppes SC. Bone and joint infections. In: Comprehensive Pediatric Hospital Medicine, 2nd ed, Zaoutis LB, Chiang WV (Eds), McGraw Hill Education, New York 2018. p.566.
  88. WHITE H. Roentgen findings of acute infectious disease of the hip in infants and children. Clin Orthop 1962; 22:34.
  89. Hefke HW, Turner VC. The obturator sign as the earliest roentgenographic sign in the diagnosis of septic arthritis and tuberculosis of the hip. J Bone Joint Surg 1942; 24:857.
  90. Chont L. Roentgen sign of early suppurative arthritis of the hip in infancy. Radiology 1942; 38:708.
  91. Jaramillo D, Dormans JP, Delgado J, et al. Hematogenous Osteomyelitis in Infants and Children: Imaging of a Changing Disease. Radiology 2017; 283:629.
  92. Gordon JE, Huang M, Dobbs M, et al. Causes of false-negative ultrasound scans in the diagnosis of septic arthritis of the hip in children. J Pediatr Orthop 2002; 22:312.
  93. Strouse PJ, DiPietro MA, Adler RS. Pediatric hip effusions: evaluation with power Doppler sonography. Radiology 1998; 206:731.
  94. Kocher MS, Mandiga R, Murphy JM, et al. A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect on outcome of septic arthritis of the hip. J Bone Joint Surg Am 2003; 85-A:994.
  95. Paisley JW. Septic bursitis in childhood. J Pediatr Orthop 1982; 2:57.
  96. Yang WJ, Im SA, Lim GY, et al. MR imaging of transient synovitis: differentiation from septic arthritis. Pediatr Radiol 2006; 36:1154.
  97. Hunter S, Kennedy J, Baker JF. External Validation of an Algorithm to Predict Adjacent Musculoskeletal Infection in Pediatric Patients With Septic Arthritis. J Pediatr Orthop 2020; 40:e999.
  98. Connolly LP, Connolly SA. Skeletal scintigraphy in the multimodality assessment of young children with acute skeletal symptoms. Clin Nucl Med 2003; 28:746.
  99. Expert Panel on Pediatric Imaging, Shet NS, Iyer RS, et al. ACR Appropriateness Criteria® Osteomyelitis or Septic Arthritis-Child (Excluding Axial Skeleton). J Am Coll Radiol 2022; 19:S121.
  100. Wilson DJ. Soft tissue and joint infection. Eur Radiol 2004; 14 Suppl 3:E64.
  101. Morrey BF, Bianco AJ Jr, Rhodes KH. Septic arthritis in children. Orthop Clin North Am 1975; 6:923.
  102. Lyon RM, Evanich JD. Culture-negative septic arthritis in children. J Pediatr Orthop 1999; 19:655.
  103. Greenwood BM, Whittle HC, Bryceson AD. Allergic complications of meningococcal disease. II. Immunological investigations. Br Med J 1973; 2:737.
  104. Rush PJ, Shore A, Inman R, et al. Arthritis associated with Haemophilus influenzae meningitis: septic or reactive? J Pediatr 1986; 109:412.
  105. Ahmed S, Ayoub EM. Poststreptococcal reactive arthritis. Pediatr Infect Dis J 2001; 20:1081.
  106. Viani RM, Bromberg K, Bradley JS. Obturator internus muscle abscess in children: report of seven cases and review. Clin Infect Dis 1999; 28:117.
  107. Song J, Letts M, Monson R. Differentiation of psoas muscle abscess from septic arthritis of the hip in children. Clin Orthop Relat Res 2001; :258.
  108. Harwell JI, Fisher D. Pediatric septic bursitis: case report of retrocalcaneal infection and review of the literature. Clin Infect Dis 2001; 32:E102.
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References

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