ESPID Reports and Reviews

Treatment of Acute Septic Arthritis

Markus Pkknen, MD* and Heikki Peltola, MD

Abstract: Acute septic arthritis is a rare, but

potentially devastating disease. The treatment is
initiated intravenously, but can be safely switched
to oral after 24 days providing large doses of a
well-absorbing antibiotic and, for time-dependent
antibiotics, 4 times-a-day administration are used.
Empiric treatment should always cover Staphylococcus aureus and common respiratory pathogens, whereas Kingella kingae and Salmonella
are important only regionally. Studies conducted
by our group have shown that a total course of 10
days may suffice for previously healthy children in
a Western setting. Treatment of neonates, patients
with immunodeficiency or cases caused by methicillin-resistant S. aureus, may deserve a different
approach.
Key Words: septic arthritis, child, Staphylococcus
aureus, clindamycin, C-reactive protein
(Pediatr Infect Dis J 2013;32: 684685)

cute septic arthritis (SA) in children is

most often of hematogenous origin. In
a Western setting, the annual incidence is
around 4:100,000 children.1 Boys are more
prone than girls. Hip, knee and ankle joints
are frequently affected. Staphylococcus
aureus is the most common causative agent,
followed by respiratory pathogens Streptococcus pyogenes, Streptococcus pneumoniae
and Haemophilus influenzae type b (Hib).24
Kingella kingae and Salmonella spp. are
regionally important agents.

DIAGNOSIS
An acutely swollen, red, painful joint
combined with high fever signal a potential
SA. Movement is limited in the affected joint
and symptoms tend to increase progressively.
The child refuses weight-bearing when the
lower limb is involved. This classical pattern
is often seen in cases caused by S. aureus,
but in contrast SA caused by K. kingae may
develop insidiously. The characteristic signs
of SA may be difficult to detect in a child
with a septic hip joint, but neonates often
assume a characteristic position with the hip
joint flexed and externally rotated. Serum
C-reactive protein (CRP) and erythrocyte
sedimentation rate are sensitive in diagnostics, but erythrocyte sedimentation rate alternates too slowly to be of much use in the follow-up.1,5 Procalcitonin challenges CRP, but
the measurement requires more time (CRP
only needs a few minutes) and is more expensive.1 Ultrasound detects joint effusion and
can guide a diagnostic joint puncture, which
should always be attempted.4 In younger children, the procedure is performed under anesthesia. A purulent joint discharge, positive
Gram stain and/or bacterial culture confirm
the diagnosis, whereas a traditional synovial
fluid cytology is often difficult to interpret
due to considerable overlap between different types of arthritides.1 In addition to conventional agar plates, aerobic blood culture
bottles are required to detect K. kingae, and
although special techniques are not required,
an automated system with capability to detect
this pathogen should be used.

TREATMENT
From the *Department of Orthopaedics and Traumatology, University of Turku, Turku University
Hospital, Turku; and Department of Pediatrics,
University of Helsinki, Childrens Hospital, Helsinki University Central Hospital, Helsinki, Finland.
M.P. received funding support from Foundation for
Pediatric Research, Finland, and Turku University
Hospital Foundation for Education and Research.
H.P. received funding support from Foundation
for Pediatric Research, Finland. H.P. works as a
consultant for Serum Institute of India Ltd. The
authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Markus Pkknen, MD,
Turku University Hospital, PO Box 52, 20521 Turku,
Finland. E-mail: Markus.Paakkonen@helsinki.fi.
Copyright 2013 by Lippincott Williams & Wilkins
ISSN: 0891-3668/13/3206-684
DOI: 10.1097/INF.0b013e31828e1721

Intravenous antibiotic is instituted

almost always before the causative agent has
been identified by cultures. The role of S.
aureus is overwhelming and its local resistance pattern dictates the choice of antibiotic.1
Large doses of clindamycin (40mg/kg/day
divided in 4 equal doses, qid) or a first-generation cephalosporin (150mg/kg/day, qid)
have been our choices against methicillinsensitive S. aureus strains,5 but staphylococcal
penicillins would likely work as well unless
exceptionally large oral doses lead to diarrhea.
The same dosing applies to both parenteral
and oral administration. If a first-generation
cephalosporin is not available for intravenous
administration, a second-generation cephalosporin may also be used as a substitute.

Clindamycin continues to be effective

against most methicillin-resistant S. aureus
(MRSA) strains.6 Clindamycin and vancomycin are ineffective against K. kingae for
which -lactams are good choices. Interestingly, cheap trimethoprim-sulfamethoxazole
is experiencing a renaissance in the treatment
of MRSA.7 Vancomycin should be considered
if resistance to clindamycin is common.2,8 An
expensive alternative is linezolid.8 Pneumococcus and S. pyogenes do not usually cause
problems in terms of resistance when high
doses are used. Hib has largely vanished from
the etiology of SA in regions with large-scale
vaccinations. If this is not the case, unvaccinated children younger than 5 years should
receive concomitant ampicillin/or amoxicillin until the agent is identified.5
The optimal duration of intravenous
and oral treatment has been disputed for decades.3,4 Severity of complications associated
with SA has led many authors to recommend
months long medications with an initial intravenous period even for several weeks.1,2,4 In a
recent study, the majority of cases of SA were
treated 3 to 5 days intravenously followed by
3 weeks of oral antibiotics.3 Current Infectious Diseases Society of America guideline
for MRSA SA states that the exact duration of
therapy should be individualized, but typically
a minimum of 3 to 4 weeks is recommended.8
In our prospective, randomized trial, a total
of 10 days of high-dose clindamycin or a
first-generation cephalosporin was sufficient
in uncomplicated cases caused by methicillin-sensitive S. aureus.4,5 The treatment was
started intravenously, usually for no more
than 2 to 4 days, and the course was completed orally to a total duration of 10 days.
One lesson learned from our largest-todate trial4 was that CRP was of great value, not
only in the diagnostics but also in monitoring
the course of illness, and in the decision to discontinue antibiotics. Our cutoff level was set at
20mg/L; once this level was reached, the medication was stopped, provided most symptoms
and signs had subsided. This occurred usually in a week or so. In cases of concomitant
osteomyelitis, we routinely extended the total
course to 20 days. Our treatment algorithm is
depicted in Figure 1.
It should, however, be kept in mind
that a 10-day treatment course is not an universally accepted standard of care, 1 of the
reasons being that it has not yet been tested

The ESPID Reports and Reviews of Pediatric Infectious Diseases series topics, authors and contents are chosen and approved
independently by the Editorial Board of ESPID.

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The Pediatric Infectious Disease Journal Volume 32, Number 6, June 2013

The Pediatric Infectious Disease Journal Volume 32, Number 6, June 2013

in MRSA cases. We therefore recommend, at

least so far, our 10-day course only for previously healthy children beyond neonatal age
whose SA is not due to agent such as Salmonella (uncommon in Western settings). These
patients, as the neonates and those with an
immunocompromise, likely need treatment
to be individually tailored. Nonsteroidal
anti-inflammatory agents are administered
at the discretion of the attending physician.
Adjuvant dexamethasone seems to slightly
quicken recovery without reducing the frequency or extent of complications.9

COMPLICATIONS
Because a dismal outcomedeath,
avascular necrosis of the femoral head,
arthrosis, an so onmay still be the ultimate
outcome of complicated SA, some further
aspects have to be taken into account. The
prognosis worsens if a child presents late
after significant cartilage destruction has

developed. Already a delay of more than 5

days from the onset of symptoms seems to
affect adversely on recovery,4 and such a
wait is regrettably common in developing
countries. In the United States, the MRSAUSA300 strain and Panton-Valentine leukocidin gene have associated with a severe
disease with a longer duration of fever.2
Extended antibiotic treatment for MRSA has
been recommended, but prospective trials are
lacking.2,8 In our series, methicillin-sensitive
S. aureus cases were treated as those caused
by other agents, and there was no difference
in outcome.10

OUR PRACTICAL APPROACH TO

TREATMENT AND CONCLUSIONS
Our approach to potential childhood SA
is straightforward: a diagnostic joint aspiration
(under anesthesia at least in younger children)
is performed and if SA is diagnosed, clindamycin or a first-generation cephalosporin is

FIGURE 1. Algorithm for determining the length of the intravenous and total antibiotic treatment in childhood acute osteoarticular infections. D indicates days.
2013 Lippincott Williams & Wilkins

ESPID Reports and Reviews

instituted, first intravenously for a few days,

then orally to a minimum of 10 days. However,
exceptionally large doses (40 or 150mg/kg/
day till a maximum daily dose of 24g or~3g,
respectively) and a qid regimen are used for
these time-dependent antibiotics.1,4,5 Once
CRP has declined below 20mg/L, the antibiotic can usually be discontinued if most symptoms and signs are alleviated. Patients who
have not responded uneventfully may benefit
from prolonged treatment. Because sequelae
may develop insidiously, a follow-up for at
least a year is well-founded.4,5
All this said, complications or deviations from the expected course of disease
occur in medicine. However, the difficult-totreat cases present a minority and can usually
be detected by simple tools such as sequential
CRP determinations.4
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Management of osteoarticular infections caused
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