Indian J Pediatr

DOI 10.1007/s12098-015-1816-1

REVIEW ARTICLE

Bone and Joint Infections in Children: Septic Arthritis

Anil Agarwal 1 & Aditya N. Aggarwal 2

Received: 9 March 2015 / Accepted: 9 June 2015

# Dr. K C Chaudhuri Foundation 2015

Abstract The pathological invasion of a joint and subsequent aspiration can be a practical alternative in case the lesion is
inflammation is known as septic arthritis. The knee and hip are diagnosed early, with uncomplicated presentations and super-
the most frequently involved joints. Staphylococcus aureus is ficial joints.
the most common cause of septic arthritis in children.
An acute onset of illness with an inflamed painful joint Keywords Septic arthritis . Pyogenic arthritis . Suppurative
and restricted movements and inability to use joint arthritis . Musculoskeletal infections . Children
(pseudoparalysis) clinically indicates septic arthritis. The di-
agnosis is difficult in a neonate or young child where refusal to
feed, crying, discomfort during change of diaper (if hip is Introduction
involved) or attempted joint movement may be the only find-
ings. Fever and other systemic signs may also be absent in The pathological invasion of a joint and subsequent inflam-
neonates. Septic arthritis is diagnosed clinically, supported by mation is known as septic arthritis. It is also commonly known
appropriate radiological and laboratory investigations. The as pyogenic arthritis or suppurative arthritis [1]. In clinical
peripheral blood white cell count is frequently raised with a practice, the diagnosis of septic arthritis is based on isolation
predominance of polymorphonuclear cells. The acute phase of causative organism from the joint fluid or positive blood
reactants such as C-reactive protein (CRP) and erythrocyte cultures plus clinical and/or radiological signs and symptoms
sedimentation rate (ESR) are often markedly raised. Ultraso- consistent with septic arthritis.
nography and MRI are preferred investigations in pediatric
septic arthritis. Determination of infecting organism in septic
arthritis is the key to the correct antibiotic choice, treatment Etiopathogenesis
duration and overall management. Joint aspirate and/or blood
culture should be obtained before starting antibiotic treatment. The bacterial seeding commonly occurs by hematogenous
Several effective antibiotic regimes are available for managing dissemination and subsequent lodging in highly vascular joint
septic arthritis in children. Presence of large collections, thick synovium. In some joints (e.g., hip, shoulder, ankle and el-
pus, joint loculations and pus evacuating into surrounding soft bow), the initial infective focus may be in the metaphyseal
tissues are main indications for surgical drainage. Joint region but the joint gets secondarily infected as the metaphysis
is within the joint. In neonates and children less than 18 mo,
transphyseal blood vessel communications allow free commu-
* Anil Agarwal nication through physeal plate and therefore infection in
rachna_anila@yahoo.co.in metaphysis can infect the joint and vice versa [2]. Other rare
causes of septic arthritis are surgeries on joints (e.g., arthros-
1
Department of Orthopedics, Chacha Nehru Bal Chikitsalaya, Geeta copy), penetrating trauma, bites or intra-articular injections.
Colony, Delhi 110031, India The numbers, type and virulence of the organism and the
2
Department of Orthopedics, UCMS and GTB Hospital, local and general resistance of the child determine the overall
Shahdara, Delhi, India outcome in septic arthritis [1]. Several possible mechanisms
 Indian J Pediatr

operate in joint destruction following septic arthritis. Firstly, There are increasing reports of an aggressive form of septic
joint damage can result from invading bacteria and its endo- arthritis being caused by pvl + or USA300 genotype contain-
toxins. Secondarily, host inflammation is believed to play a ing methicillin-resistant Staphylococcus aureus (MRSA)/
significant role in joint damage following septic arthritis [3]. methicillin-sensitive Staphylococcus aureus (MSSA) from
This can occur even though bacteria have been killed. Another western countries especially United States (USA) [12].
factor responsible for joint destruction is joint ischemia. The Panton-Valentine leukocidin (pvl) is a cytotoxin encoded by
infectious process induced joint effusion may produce pvl genes that destroys leucocytes by creating pores in the cell
tamponade of the nutrient blood vessels, ischemia, articular membrane. More than 90 % of MRSA isolates are related to a
cartilage and capsular destruction. This mechanism becomes USA300 clone which frequently carries both pvl and fnbB
more important in deep joints such as hip. genes encoding for fibronectin binding factor. This protein is
associated with enhanced bacterial adhesion and invasion.
Following infection with this peculiar organism, an aggressive
Epidemiology and Causative Organisms type of septic arthritis manifests with increased incidence of
severity and virulence, higher incidences of bacteremia and
The estimated annual incidence of septic arthritis in the children osteomyelitis (>30 %), pyomyositis/myositis or cellulitis, sep-
ranges between 5 and 12 cases per 100,000 persons although it tic thrombophlebitis, endocarditis and septic pulmonary em-
varies in different world geographic regions [4]. In many devel- boli. Children suffering with pvl + or USA300 Staphylococcus
oped regions of the world (e.g., Israel), the incidence of septic aureus septic arthritis are more seriously ill, have higher and
arthritis in children is very low (1 in 100,000) [5]. On the other prolonged fever, greater tachycardia, greater disability to bear
hand, in some developing countries of Africa, the incidence of weight, profound leukocytosis and thrombocytosis, inflated
septic arthritis is high (5–20 in 100,000) [6]. Staphylococcus is serum inflammatory markers (CRP and ESR) and a depressed
the most common cause of septic arthritis in children and ac- hematocrit, and they require a longer hospital stay [12, 13].
counts for 25–60 % culture positive cases [2, 7]. The age wise In some tropical countries (e.g., Kenya, Malawi and Zam-
common causative pathogens are listed in Table 1. bia), Salmonella induced septic arthritis is common with sick-
Hip and knee are the most frequently involved joints. Other le cell disease, anemia, poor nutritional status and malaria
joints commonly involved are ankle, elbow, shoulder, sacroil- being important risk factors [6].
iac and metatarsophalangeal joints [7]. In certain geographic
areas e.g., Africa, there is predisposition to involvement of
shoulder joint [6]. Most cases are monoarticular (90 %) al- Clinical Presentation and Diagnosis
though polyarticular presentations do occur.
Several risk factors for septic arthritis have been identified An acute onset of illness with an inflamed painful joint and
viz. young age (3 y or younger), male gender, trauma, weak- restricted movements clinically indicates septic arthritis unless
ened immune system due to any reason (under development, proved otherwise. Child or parents may give history of prior
prematurity, low birth weight, sickle cell disease, hemophilia trauma or upper respiratory tract illness. The child with septic
and/or HIV positive), respiratory distress syndrome and um- arthritis usually has a sick appearance. In general, the features
bilical artery catheterization [9]. of septic arthritis are sudden onset of fever, pain, irritability,
In approximately 18–70 % cases, no organisms can be inability to use the joint (pseudoparalysis). The clinical pre-
identified (culture negative septic arthritis) [7, 10]. The possi- sentation will vary depending upon the age of the child, the
ble explanations for culture negative results are mistaken di- extremity affected and the location of the joint (superficial/
agnosis; small bacterial load in sample; requirement of more deep). In lower extremity, pain and limp are the predominant
sensitive diagnostic methods or samples obtained after initia- symptoms. In affection of the hip joint, the limb assumes the
tion of antibiotics. It appears likely that many children previ- attitude of flexion, abduction and external rotation. There is
ously marked as Bculture negative^ septic arthritis are infected both active and passive restriction to move the joint. The child
with Kingella kingae [11]. In fact, Kingella kingae is increas- often refuses to walk. External swelling may not be an early
ingly becoming an important organism in etiology of feature of septic arthritis especially in deep seated joints such
osteoarticular infections under the age of 3 y. as hip. Sometimes the hip pain is referred to groin, thigh or
Septic arthritis due to Haemophilus influenzae has become knee. In advanced presentation, the abscess may burst out of
rare in countries where immunization coverage is high [8]. hip capsule and lie in soft tissues. Joint instability may be seen
When present, children with Haemophilus influenzae septic in such cases. In a superficial joint such as knee and shoulder
arthritis frequently present with multifocal disease with other or elbow, erythema, swelling, and warmth may be quite obvi-
suppurative foci of infection such as meningitis (30 % of pa- ous. The diagnosis is essentially difficult in a neonate or
tients), osteomyelitis (22 %), cellulitis (30 %), pneumonia young child where refusal to feed, crying, discomfort during
(4 %), and otitis media (35 %) [8]. any attempted movement of the joint e.g., change of diaper (if
Indian J Pediatr

Table 1 Child’s age and common pathogens responsible for septic arthritis [8]

Organisma

Age
Infant 0–2 mo Staphylococcus aureus
Streptococcus agalactiae
Gram negative enteric bacteria
Coagulase negative staphylococci
Neisseria gonorrhoeae
Candida
Streptococcus pneumoniae
2 mo–5 y Staphylococcus aureus
Streptococcus pyogenes
Streptococcus pneumoniae
Kingella kingae
Haemophilus influenzae type b (in non-immunized child)
>5 y Staphylococcus aureus
Streptococcus pyogenes
Adolescent Neisseria gonorrhoeae
Associated with immunosuppression C. immitis
B. dermatitis
H. capsulatum
C. neoformans
Gram negative bacteria
Possible causes in endemic areas
Tick exposure Borrelia burgdorferi (Lyme disease)
Travel/contact Mycobacterium tuberculosis
Rat exposure Streptobacillus moniliformis
Rare causes (All age groups) Viral (Rubella, parvovirus B19, varicella zoster, hepatitis), Candida, anaerobes, Brucella

The list is not exhaustive and may vary from regions and health centres
a
S. pyogenes Group A streptococci (A subgroup of Beta hemolytic streptococci)
S. agalactiae Group B streptococci (A subgroup of Beta hemolytic streptococci)

hip is involved) may be the only findings. Fever and other test [14]. Serum alkaline phosphatase is another new ex-
systemic and local signs may be absent in neonates. Hence a perimental indicator in acute bone and joint infections
high index of clinical suspicion has to be kept in neonates. [15]. After the decrease seen during the first few days
Common differential diagnosis of septic arthritis in children of infection, a constantly increasing alkaline phosphatase
include acute osteomyelitis, cellulitis, reactive arthritis, juve- levels were seen in the following few weeks, regardless
nile rheumatoid arthritis, trauma, neoplasia and hemarthrosis. of diagnosis, antibiotic administration, and duration of
In hip, transient synovitis (toxic synovitis), Legg-Calve- antibiotic administration possibly because alkaline phos-
Perthes disease and slipped capital femoral epiphysis can have phatase elevation may be part of the natural healing pro-
initial presentation similar to septic arthritis. cess in bone and joint infections [15]. More recently,
Septic arthritis is diagnosed clinically, supported by leukocyte esterase analysis of joint fluid and serum
appropriate radiological and laboratory investigations. procalcitonin have been included as new research tools
The peripheral blood white cell count (WBC) is fre- to diagnosis native joint infections [16]. However, one
quently raised with a predominance of polymorphonucle- should take caution that these hematological parameters
ar cells. The acute phase reactants such as C-reactive can be within normal limits in septic arthritis (e.g., CRP
protein (CRP) and erythrocyte sedimentation rate (ESR) may be normal in infection with Kingela kingae) [17].
are often markedly raised. Other markers of limited di- CRP response is acutely elevated in septic arthritis
agnostic value are synovial fluid/serum glucose ratio be- compared to osteomyelitis [17]. CRP peaks within
low 0.5, increased synovial lactate, and a positive mucin 48 h of onset but ESR generally peaks at 3 to 5 d. In
 Indian J Pediatr

uncomplicated infections, CRP declines within 6 h of Some organisms require other investigations for their
effective antibiotic therapy and generally returns to nor- detection. If Neisseria gonorrhoeae is suspected, cul-
mal within 7 to 10 d. The return to normal values of tures of joint fluid, blood, pharynx, skin lesions and
ESR is delayed and may take upto 6 wk [7]. genitourinary source should be obtained and inoculated
Many algorithms based on acute inflammatory on enrichment media. A throat culture for Streptococcus
markers have been utilized for ruling out the diagnosis pyogenes should be sent if patient has signs and symp-
of septic arthritis [8]. If CRP and ESR remain normal toms of pharyngitis. Antistreptolysin O and anti-DNase
for 3 d after admission, osteoarticular infection is un- B may provide corroborative evidence in Streptococcus
likely to be present [18]. A recent study has postulated pyogenes infection. Certain Kingella kingae clones pro-
that if ≥3 criteria (age above 3.6 y, CRP>13.8 mg/L, duce an RTX (repeats-in-toxin) toxin responsible for
duration of symptoms >3 d, platelets<314×10 cells/μL, mucosal colonization, bacteremia and infections which
and acute neutrophil count>8.6×10 cells/μL) are pres- require use of blood culture bottles and PCR-based assays
ent, it is predictive of adjacent infections and an MRI [23].
scan is warranted in such cases [19]. In another study, Plain radiography is not particularly helpful in early stages
CRP>20 mg/L, non-weight-bearing, temperature >38.5 ° of septic arthritis. An increased joint space can be appreciated
C and peripheral white blood cell count>12×109 cells/L in cases of joint effusion [24]. There can be periarticular soft
offers a predictive probability for septic arthritis of tissue changes in some patients. Concomitant osteomyelitis,
87 % [20]. A secondary CRP rise may be an important fractures and neoplasia can be differentiated from septic ar-
sign of recurrence of osteoarticular infections. The thritis on plain radiographs. With joint destruction, joint irreg-
treating clinician however must exert caution while ularities, subluxations and dislocation become obvious on
using such algorithms in neonates and children. Because plain radiographs.
of a poorly developed immune system, many Many centers now rely on ultrasonography to detect joint
osteoarticular infections in pediatric age group (e.g., effusions and it has emerged as preferred investigation in pe-
Kingela kingae) may not induce an expected body reac- diatric hip septic arthritis [25]. It has high sensitivity and fluid
tion and the inflammatory markers like WBC count and effusions as low as 1–2 ml can be detected. Ultrasound can
ESR may be within normal limits [8, 21]. also guide needle aspirations of deep joint, especially hip [25].
If septic arthritis is suspected, a joint aspiration is However, ultrasound may be negative in early septic arthritis
mandatory irrespective of the age of the child. (<24 h) when significant joint effusion has not accumulated.
Performing an image guided aspiration increases the Ultrasound is an operator dependent modality and requires
yield and accuracy of the aspirate especially for a deep training and experience. Further, ultrasound cannot distin-
joint such as hip. Despite a negative aspirate, where guish between infective and non infective collections (such
clinical suspicion of septic arthritis is strong, a surgical as juvenile arthritis).
arthrotomy is indicated to obtain joint fluid and tissue Magnetic resonance imaging (MRI) is also a good
for laboratory analysis. The aspirated joint fluid should modality to substantiate the diagnosis of septic arthritis.
be sent for cytological and biochemical analysis, Gram If a child fails to respond to appropriate antibiotic ther-
staining and aerobic and anaerobic cultures. Many cen- apy within 48 h, MRI should be considered to identify
ters have started testing this material for fungal and associated osteomyelitis [26]. MRI findings in septic
tubercular organisms as well. In an appropriate clinical arthritis include signal intensity changes in the bone
setting, a synovial fluid WBC count of ≥50,000/mm3 marrow and adjacent soft tissues. Contrast enhancement
with raised polymorphonuclear cells (>90 %) is highly may also be present in surrounding soft tissues. Other
indicative of septic arthritis [22]. pathologies such as transient synovitis of hip will have
Gram staining of joint fluid is positive for organisms no signal alterations in bone marrow or less likely in
in approximately 30 % cases only [9]. The yield can be adjacent soft tissues. CT scans can also detect effusions
increased if synovial tissue is also cultured for organism and guide joint aspirations in septic arthritis but are
isolation and identification. The blood cultures may be considered inferior to MRI for septic arthritis. Bone
positive (22 %) even when joint aspirates are negative. scans are especially useful in locating multifocal septic
Dedicated laboratories with facilities of enrichment me- arthritis seen in neonates and MRSA cases.
dia for fastidious bacteria, polymerase chain reaction
(PCR) and 16S rDNA PCR to detect microbial specific
antigens are important for organism identification and Treatment
determination of antibiotic sensitivity [8]. The results
of rapid PCR based assays are available in approximate- Determination of infecting organism in septic arthritis is
ly 3 h compared with 1–2 d with routine cultures [8]. the key to the correct antibiotic choice, treatment
Indian J Pediatr

Suspect: Child with fever, solitary joint pain, swelling, tenderness, limited ROM, limp, or afebrile neonate with extremity disuse

Labs: CBC, DLC, ESR, CRP, blood cultures. Radiographs of involved joint.

If clinical Surgical evacuaon of joint or aspirated to dryness. Send specimen for microbiological &
dilemma persists, MRI, histopathological analysis. Iniate IV anbiocs as per local flora & AB policy.
aspiraon under US/CT; If delay in laboratory/ imaging/ surgical procedures ancipated, iniate empirical anbiocs
Repeat CRP on clinical judgment.

Discharge criteria: afebrile x 24-48h, clinical and lab

US/MRI (+) for joint US/ MRI (-) for joint Exclude sepc arthris (of hip) parameters supporve
effusion or metaphyseal effusion or if T>38.50C, elevated CRP, non-
osteomyelis metaphyseal wt bearing
osteomyelis Sequenal follow
up
Joint Observe clinical course.
aspiraon: Monitor blood cultures,
Gm stain, lab parameters. Re-
joint cell evaluate.
count,
culture, PCR

Gm stain (+) or
Gm stain (-) clinical suspicion of
SA

Monitor clinical
course over next 48h

If clinical deterioraon,
consider surgery

Fig. 1 Septic arthritis in a child-management algorithm [8]

duration and overall management (Fig. 1) [8]. The treat- The ‘Correct’ Antibiotics
ment will depend upon the severity of infection, number
of joints involved and associated risk factors. Thus, ev- Several effective antibiotic regimes are available for managing
ery effort should be made for identification of causative septic arthritis in children (Table 2) [8].
organism. Blood cultures and joint fluid aspirates for The choice of antibiotics should be judicious and based on
biochemical and microbiological analysis and culture the microbial profile in the region. It should take into account
must be obtained prior to starting any antibiotic treat- patient’s age, antibiotic availability and socioeconomic
ment. Before the laboratory reports are available, the considerations.
antibiotic treatment is initiated for the most likely path- In neonates (<28-d-old), Group B streptococcus, Staphylo-
ogen based on clinical findings and regional microbio- coccus aureus and gram negative organisms are potential
logical profile. The antimicrobial drugs are changed af- pathogens and therefore, empirical therapy including oxacillin
ter the causative organism and its drug sensitivity has or cefotaxime with addition of gentamicin is recommmended
been determined. Intraarticular injection of antibiotics is [27, 28]. If MRSA is not a concern, the empirical therapy for
not advocated. children 3 mo or older would be antistaphylococcal penicillin
There is much controversy in the literature regarding (nafcillin or oxacillin) or Ist generation cephalosporin
the choice of antibiotic to be used, route of antibiotic (cefazolin) [27]. This therapy covers ordinary MSSA, Strep-
delivery—intravenous vs. oral, factors determining tococcus pyogenes and Kingella kingae. If MRSA prevalence
switching over to oral antibiotics and duration of antibi- is >10 % (some experts say 25 %), the empirical antibiotic
otic usage [20]. No consensus has been formed world- choice is vancomycin or clindamycin [8]. Clindamycin is the
wide regarding the above issues. One probable reason for first preference antibiotic for MRSA induced septic arthritis
these variations is different organism profile and the when Staphylococcus isolate is susceptible to it. If local
resulting severity of septic arthritis. clindamycin resistance rates are >10–25 %, or in a setting of
 Indian J Pediatr

Table 2 Commonly used antibiotics in septic arthritis in children [8]

Organism considerations Intravenous antibiotics Follow up oral agent in susceptible isolates

1st line 2nd line/resistance to 1st line

MSSA Flucloxacillin and Gentamicin Cefotaxime Cephalexin

Nafcillin/Oxacillin Ceftriaxone Dicloxacillin/Cloxacillin/Flucloxacillina
Cloxacillincefa Clindamycin Coamoxyclav
Zolin Cefuroxime Cephadroxil
Coamoxyclav Clindamycin
Fuscidic acid Cefuroxime
Cephradrine
Cephalothin
Ampicillin–Sublactum
Vancomycin
MRSA Clindamycinb Vancomycin Clindamycin
Linezolid Linezolid
Trimethoprim-Sulfamethoxazole Trimethoprim-Sulfamethoxazole
Minocycline
Doxycycline
Daptomycin
Kingella kingae Penicillin G Cefotaxime Cefuroxime
Cefazolin Ceftriaxone
Cefuroxime
Group A streptococcus (GAS) Penicillin G Ampicillin Clindamycin
Cefazolin
Clindamycin
Group B streptococcus Penicillin G Oxacillin Clindamycin
Cefotaxime Ampicillin
Ampicillin
Cefazolin
Clindamycin
Streptococcus pneumoniae Penicillin G Cefotaxime Coamoxyclav
Ceftriaxone Clindamycin
Coamoxyclav
Clindamycin
Vancomycin
Pseudomonas Flucloxacillin and Gentamicin Cefepime
Ceftazidime Piperacillin
Imipenem
Azetreonam
Gram negative bacteria Gentamicin Cefuroxime Cefuroxime
Cefotaxime
Ceftazidime
Tobramycin
Hemophilus influenza Ampicillin Cefuroxime Cefuroxime
Ceftriaxone Amoxillin
Ampicillin
Neisseria gonorrhoeae Ceftriaxone Ampicillin Ampicillin
Cefotaxime
Salmonella Flucloxacillin and Ampicillin Ampicillin
Cefotaxime
Ceftriaxone

Combinations may be used. The list is not exhaustive and may vary from regions and health centers
a
β-lactamase resistant penicillin: Cloxacillin (Dicloxacillin, Flucloxacillin), Nafcillin, Oxacillin, Methicillin. Nafcillin therapeutically equivalent to
Oxacillin, Methicillin. Dicloxacillin and Flucloxacillin are again considered very similar
b
Check for inducible macrolide-lincosamide-streptogramin B phenotype (MLSB phenotype) when using Clindamycin. If present, Clindamycin usage is
not preferred

clindamycin inducible resistance, vancomycin should be used. Kingella kingae. Cefazolin should be added if Kingella kingae
Both vancomycin and clindamycin are not effective against is also suspected in etiology. Once the organism is isolated and
Indian J Pediatr

antibiotic sensitivity has been determined, the initial empirical Studies from Finland indicate that shorter antibiotic re-
antibiotics may be modified accordingly. The therapy may be gimes up to 10 d with intravenous drug administration being
stepped to oral therapy with cephalexin or dicloxacillin in 2–4 d and rest orally, might suffice in uncomplicated MSSA
methicillin sensitive isolates [29]. Another alternative is oral cases and other bacterial infections [7]. If adjacent bone is
clindamycin in cases of allergy to β lactum antibiotics or affected, treatment is extended for approximately 20 d. If
when isolate is MRSA. most (if not all) symptoms and signs subside within a few
days, and the serum CRP falls below 20 mg/dl, the antibiotics
The ‘Correct’ Duration can safely be discontinued [7]. These guidelines are, however
not rigid and require individualization depending upon sever-
Intravenous Therapy ity of infection, organism, regional sensitivity patterns, time
elapsed between onset of symptoms and child’s presentation
There is an ongoing debate on the recommended duration of and the clinical and laboratory responses to the treatment
intravenous therapy, with ranges from 2 to 7 wk [30]. Some [35].
studies have recommended shorter intravenous regimens (2–
7 d) followed by 2–4 wk of oral therapy for uncomplicated Surgical Intervention
septic arthritis [31, 32]. Prolongation of antibiotic treatment is
often needed if there is failure of response to initial drainage Presence of large collections, thick pus, joint loculations
and intravenous antibiotics, there has been delay or incom- and pus evacuating into surrounding soft tissues are main
plete surgical evacuation of pus or if there are other foci of indications for surgical drainage [36]. In view of devas-
infection in disseminated staphylococcal disease e.g., endo- tating sequelae of post septic arthritis pediatric hip (and
carditis, osteomyelitis [33]. Treatment in newborns, immuno- sometimes shoulder), arthrotomy is justified even on
compromised patients or infection with Salmonella may also strong clinical suspicion. Joint aspiration can be a practi-
require prolonged treatment [7]. In a prospective evaluation, cal alternative in case the lesion is diagnosed early (<4 d),
Jagodzinski et al. showed that a temperature greater than 38.4° with uncomplicated presentations and superficial joints
and CRP >10 mg/dl on admission predicted a longer duration [7]. An experienced clinician should be available and ul-
of intravenous antibiotic [31]. trasound guided aspirations are preferred in such cases
[38]. Daily aspirations may be required initially till joint
Switch Over to Oral Therapy is dry. Where specialized facilities and equipment is avail-
able, arthroscopic joint drainage (shoulder, elbow, knee,
Generally oral therapy is begun with settling of temperature ankle) can be used [39]. If aspiration/drainage is not
(should be declining although it may not have settled followed by a rapid reversal of clinical symptoms and
completely), child’s improving clinical status-pain, range of normalization of vital signs, it generally indicates
movement and weight bearing status and a normalizing CRP residual/multifocal or recurrence of infection and re-
[7, 34]. A switch from intravenous to oral therapy is also exploration should be considered [36]. Besides antibi-
guided by the availability of an appropriate oral antibiotic, otics, the child also requires analgesia and antipyretics.
the child’s ability to take oral medication, gastrointestinal tol- Early physical therapy and aggressive mobilization of
erance for high dose of antibiotics, reliable caregivers and joint is initiated as soon as pain permits and infection is
possible observation of child at scheduled periods to assess under control (as early as 24 to 48 h) [8].
response [35]. Ten percent of infants and children do not re- Some studies have shown that addition of dexamethasone
spond to oral medication at all and need continuous intrave- (0.6 mg/kg per 24 h divided q8h) during the initial 4 d in the
nous antibiotic treatment [36]. management of septic arthritis decreases the duration of symp-
toms, brings about rapid clinical improvement, shortens hos-
Total Duration of Antibiotics pitalization and reduces long term joint dysfunction [40].
However, the use of corticosteroids in patients with serious
There is increasing evidence to suggest that a shortened dura- infection should be considered only after due consideration.
tion (<6 wk) of therapy does not have a deleterious effect and Acute septic arthritis of childhood is a potentially devastat-
3–4 wk of antibiotic treatment is probably adequate [37]. ing disease responsible for significant morbidity and even
Some authors have categorized the duration of antibiotic in- mortality (1–15 %) [36]. Complications are reported in 10–
take according to the pathogen. Generally, infections with 25 % of the septic arthritis cases. The risk factors for compli-
Streptococcus pneumoniae, Kingella kingae, Haemophilus cations include delay in diagnosis (>4–5 d), neonatal infec-
influenzae, and Neisseria gonorrhoeae are treated for 2– tions, infection with Staphylococcus aureus or gram negative
3 wk. Infections caused by Staphylococcus aureus, or gram bacteria and concomitant osteomyelitis [38–41]. Main com-
negative bacteria are treated for 3–4 wk [38]. plications following septic arthritis include restricted range of
 Indian J Pediatr

motion, deformities, and joint destructions. A close clinical 16. Omar M, Ettinger M, Reichling M, et al. Preliminary results of a
new test for rapid diagnosis of septic arthritis with use of leukocyte
and radiological follow up is needed for at least 6 wk after
esterase and glucose reagent strips. J Bone Joint Surg Am. 2014;96:
resolution of symptoms to check for any evidence of contin- 2032–7.
ued infection/onset of complications [30]. Serial follow up 17. Basmaci R, Ilharreborde B, Bonacorsi S, et al. Septic arthritis in
for minimum 1 y is highly desirable although sequelae of children with normal initial C-reactive protein: clinical and biolog-
septic arthritis can manifest several years after initial infection ical features. Arch Pediatr. 2014;21:1195–9.
18. Pääkkönen M, Kallio MJ, Kallio PE, Peltola H. Sensitivity
[42]. of erythrocyte sedimentation rate and C-reactive protein in
childhood bone and joint infections. Clin Orthop Relat Res.
2010;468:861–6.
Conflict of Interest None. 19. Rosenfeld S, Bernstein D, Daram S, Dawson J, Zhang W. Predicting
the presence of adjacent infections in septic arthritis in children.
J Pediatr Orthop. 2015. doi:10.1097/BPO.0000000000000389.
Source of Funding None. 20. Rutz E, Spoerri M. Septic arthritis of the paediatric hip—a review of
current diagnostic approaches and therapeutic concepts. Acta
Orthop Belg. 2013;79:123–34.
21. Yagupsky P. Letter to the editor: another look: is there a flaw to
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