Download A 34-Day-Old With Fever, Cerebrospinal Fluid

DIAGNOSTIC DILEMMAS AND CLINICAL REASONING
A 34-Day-Old With Fever,
Cerebrospinal Fluid Pleocytosis, and
Staphylococcus aureus Bacteremia
Kimberly Horner, MD,a Masaki Yamada, MD,b Giulio Zuccoli, MD,c Stacy Rosenberg, MD,d
Stephanie Greene, MD,e Kishore Vellody, MD,f Noel S. Zuckerbraun, MDa
A 34-day-old previously healthy boy born full term presented to the
emergency department with fever at home (38.1°C), fussiness, and
decreased oral intake for 1 day. He was difficult to console at home. He had
decreased oral intake without emesis, diarrhea, or a change in urine output.
He did not have rhinorrhea, cough, or increased work of breathing noted by
parents. He lived at home with his parents and 13-year-old brother, did not
attend day care, and had no sick contacts. On examination, he was fussy but
consolable. He was febrile to 39.3°C, tachycardic (180 beats per minute),
and tachypneic (64 breaths per minute), with mottling and a capillary refill
of 3 seconds. The remainder of his examination was normal, without an
infectious focus for his fever. A complete blood cell count with differential
revealed leukocytosis. A basic metabolic panel was normal. A catheter
urinalysis was normal. Cerebrospinal fluid examination yielded pleocytosis,
low glucose, and elevated protein. Blood cultures were persistently positive
with methicillin-sensitive Staphylococcus aureus, but cerebrospinal fluid
cultures remained negative. We present his case, management, and ultimate
diagnosis.
abstract
Divisions of aDepartment of Pediatrics, Emergency
Medicine, bInfectious Diseases, and dAllergy and
Immunology, fDiagnostic Referral Group, and Departments
of cRadiology and eNeurosurgery, The Children’s Hospital of
Pittsburgh of UPMC, Pittsburgh, Pennsylvania
Dr Horner conceptualized and designed this case
presentation and drafted the initial manuscript;
Drs Yamada, Zuccoli, Rosenberg, Greene, Vellody,
and Zuckerbraun contributed to the conception and
design of this case presentation and reviewed and
revised the manuscript; and all authors approved
the final manuscript as submitted.
DOI: 10.1542/peds.2015-1406
CASE HISTORY WITH SUBSPECIALTY
INPUT
Dr Kimberly Horner (Pediatric
Emergency Medicine)
A 34-day-old previously healthy boy
who was born full term presented
with fever at home (38.1°C), fussiness,
and decreased oral intake for 1
day without other accompanying
symptoms. He was difficult to console
at home. He had decreased oral intake
of formula without emesis, diarrhea,
or a change in urine output. He did not
have rhinorrhea, cough, or increased
work of breathing noted by parents.
He lived at home with his parents and
13-year-old brother, did not attend
day care, and had no sick contacts.
On initial examination, he was noted
to be febrile (39.3°C), tachycardic
(180 beats per minute), tachypneic
(64 breaths per minute), and fussy.
He had poor perfusion, with mottling
and a capillary refill of 3 seconds. The
abnormal vital signs and perfusion
improved with 40 mL/kg normal
saline bolus and acetaminophen. The
remainder of his examination was
normal, without an infectious focus
for his fever. Notably, his anterior
fontanelle was not bulging. He had
no increased work of breathing
or adventitious breath sounds, no
gallop or murmurs, no abdominal
tenderness, distention, masses, or
hepatosplenomegaly, and no rashes.
Dr Zuckerbraun, what is your
approach to a 34-day-old infant with
fever?
PEDIATRICS Volume 137, number 1, January 2016:e20151406
Accepted for publication Jul 14, 2015
Address correspondence to Kimberly Horner, MD,
Children’s Hospital of Pittsburgh of UPMC, 4401
Penn Ave, AOB 2nd Floor Suite 2400, Pittsburgh, PA
15224. E-mail: [email protected]
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online,
1098-4275).
Copyright © 2016 by the American Academy of
Pediatrics
FINANCIAL DISCLOSURE: The authors have
indicated they have no financial relationships
relevant to this article to disclose.
FUNDING: No external funding.
POTENTIAL CONFLICT OF INTEREST: The authors
have indicated they have no potential conflicts of
interest to disclose.
To cite: Horner K, Yamada M, Zuccoli G, et
al. A 34-Day-Old With Fever, Cerebrospinal
Fluid Pleocytosis, and Bacteremia. Pediatrics.
2016;137(1):e20151406
SPECIAL ARTICLE
Dr Noel Zuckerbraun (Pediatric
Emergency Medicine)
Fever is often the only presenting
sign of a serious bacterial infection
in an infant ≤60 days of age, and up
to 12% of febrile infants in this age
group have either a urinary tract
infection, bacteremia, or bacterial
meningitis. Although urinary tract
infection is the most common, 1% to
3% have bacteremia or meningitis.1–4
The standard emergent evaluation
for these infants includes obtaining
blood, urine, and cerebrospinal fluid
(CSF) studies and cultures, with
subsequent risk assignment and
management strategies based on age,
clinical assessment, and diagnostic
test results.
Empirical antibiotics to treat a
possible bacterial infection should
be considered for infants who do
not meet low-risk criteria. There are
several different published low-risk
criteria, with most criteria involving
a well-appearing, previously healthy
infant with low white blood cell
counts and negative Gram stain in the
serum, urine, and CSF and no other
focus of infection.1–3 Our patient
was not considered low-risk from
the time of his initial assessment,
because he was not well appearing
with tachycardia and poor perfusion.
Thus, along with fluid resuscitation,
antibiotics were initiated
immediately after blood, urine, and
CSF cultures were collected, before
results were obtained, and he was
admitted to the hospital. The choice
of antibiotic treatment for children
who do not meet low-risk criteria
typically includes a combination
of antibiotics targeting bacteria
that differs with the age of the
patient. Typically, ampicillin and
an aminoglycoside (ie, gentamicin)
or ampicillin and cefotaxime are
given to infants <1 month old to
treat presumptive bacteria such as
Streptococcus agalactiae, Listeria
monocytogenes, and gram-negative
species such as Escherichia coli and
Klebsiella. For infants >1 month old,
2
a third-generation cephalosporin is
given to treat presumptive bacteria,
including Streptococcus pneumoniae,
Neisseria meningitides, Streptococcus
agalactiae, Haemophilus influenzae,
and E coli. Vancomycin may be added
if bacterial meningitis is suspected.
Institutions and local community
resistance patterns may alter these
typical regimens.5
When evaluating a febrile neonate,
there is no consensus in the literature
regarding the addition of antiviral
therapy (acyclovir) for empirical
coverage of herpes simplex virus
(HSV) infection. HSV encephalitis,
though uncommon, has a similar
prevalence to bacterial meningitis
in infants ≤28 days old and has a
high morbidity and mortality.6 Twothirds of infants with HSV infection
do not have a history of parental
HSV.7–9 Therefore, some institutions
recommend starting acyclovir in
infants ≤14 days old who present
with a fever.10 Given the inability
to identify infants at low risk of
HSV infection, it is practice in our
institution to start acyclovir on
infants ≤60 days of age who present
with fever and skin vesicles, hepatitis,
seizures, aseptic meningitis (CSF
leukocytosis with negative Gram
stain), sepsis, encephalitis, or focal
neurologic findings.
Dr Horner
For this patient, a complete blood
cell count with differential revealed
leukocytosis with 17 700 white
blood cells (56% neutrophils and
4% bands). A basic metabolic
panel, catheter urinalysis, and
chest radiograph were normal. CSF
examination yielded pleocytosis
(2113 white blood cells with
66% neutrophils and 34%
monocytes), 424 red blood cells,
hypoglycorrhachia (39 mg/dL),
and elevated protein (534 mg/dL),
which raised concern for meningitis.
Blood cultures were persistently
positive over 48 hours with
methicillin-sensitive Staphylococcus
aureus (MSSA).
The patient’s CSF results raised
concern for meningitis, specifically
bacterial meningitis. He had been
empirically started on ampicillin,
cefotaxime, and acyclovir. After CSF
results were noted to be concerning
for bacterial meningitis, ampicillin
was changed to vancomycin to treat
possible pneumococcal meningitis.
The initial blood culture and a blood
culture obtained 24 hours later
resulted in positive identification
of MSSA. A blood culture obtained
48 hours after presentation was
negative. Urinalysis and CSF cultures
remained negative.
Dr Yamada, how do you interpret
the results of the CSF studies in the
setting of a negative CSF culture but
positive blood cultures for MSSA?
Given the rarity of MSSA meningitis
in this age group, what is your
differential for the source of the
infection?
Dr Masaki Yamada (Pediatric
Infectious Diseases)
The CSF results were remarkable for
neutrophil-dominant pleocytosis,
hypoglycorrhachia, very high protein,
but negative Gram stain and culture.
To clarify, the CSF was obtained
before the antibiotics were started.
This finding is consistent with
aseptic meningitis. In the presence
of persistent MSSA bacteremia,
we certainly suspected that the
inflammation of meninges was
caused by MSSA. Interestingly,
however, Staphylococcus aureus
rarely causes meningitis in otherwise
healthy people in all age groups
with the exception of patients with
devices, trauma, or surgery in the
central nervous system (CNS).5
Rather, S aureus more commonly
causes brain abscesses, infected
subdural hematomas, epidural
abscesses, infected cerebral venous
sinus thrombosis, or paraspinal
abscesses with or without CSF
pleocytosis. Therefore, we certainly
HORNER et al
had to look for a parameningeal
source of infection.
present without specific signs of bone
involvement on examination.11
Additionally, when we see a patient
with S. aureus bacteremia without
a source, we typically look for a
musculoskeletal infection such as
osteomyelitis, pyomyositis, and
septic arthritis or for an intravascular
infection such as endocarditis.
These infections are almost always
hematogenously spread, which
more often occurs in neonates
with prematurity in the NICU
as opposed to healthy full-term
infants. Unfortunately, given the
rarity of S aureus parameningeal,
musculoskeletal, and intravascular
infections in infants, the incidence is
not well described.
Dr Zuccoli, if osteomyelitis is
suspected, what imaging modalities
would you recommend for this age
group?
Dr Horner
The infant was noted to have
a transient systolic murmur
once admitted to the hospital. A
transthoracic echocardiogram
was normal. Although diagnosis
of osteomyelitis in young infants
is challenging, we thought it was
unlikely in this infant because
only 20% of infants <4 months old
Dr Giulio Zuccoli (Pediatric
Neuroradiologist)
If osteomyelitis is suspected, plain
radiography would be the first
choice to evaluate for soft tissue
swelling and changes in bone density.
However, in cases of hematogenous
osteomyelitis, it may take up to 2
weeks for plain radiography to reflect
changes suggesting osteomyelitis.
Therefore, plain radiography may
be normal in the initial phase of the
disease, which would have been the
case for this infant presenting within
the first few days of illness. Other
methods to evaluate for osteomyelitis
in infants include ultrasound, MRI,
and scintigraphy. Ultrasound and
MRI can detect changes several
days earlier than plain radiography,
although it is more useful if there
is a suspected location of infection.
Scintigraphy is more useful when the
FIGURE 2
Axial images on postcontrast T1-weighted
images better reveal the cross-sectional
area of the fluid collection (asterisk). Early
infectious involvement of the spinal cord is also
noted (arrows).
suspected location of osteomyelitis is
unknown.12,13
Dr Horner
Because the infant did not have a
suspected location of osteomyelitis,
scintigraphy would have provided
the highest yield, but given the CSF
results with neutrophil-predominant
pleocytosis, hypoglycorrhagia, and
elevated protein with negative
cultures, additional investigation
was focused on the CNS to evaluate
for a source of meningeal or
parameningeal inflammation.
A head computed tomography
scan with contrast and brain MRI
with venography did not show an
intracranial infection such as a brain
abscess. A spinal ultrasound was
negative for a paraspinal abscess.
A spine MRI with contrast was
abnormal (Figs 1 and 2).
Dr Zuccoli, can you describe the MRI
findings?
Dr Giulio Zuccoli (Pediatric
Neuroradiologist)
FIGURE 1
A, The sagittal T2-weighted image clearly reveals the dura mater (arrowheads) and shows the
anterior epidural abscess indenting the spinal cord. B, The abscess has thick enhancing walls, seen
on postcontrast T1-weighted images (arrowheads), and the vertebral body of C4 shows pathologic
contrast enhancement (arrow).
PEDIATRICS Volume 137, number 1, January 2016
The MRI of the cervical spine
demonstrated an extradural fluid
collection, which was isointense to
the CSF on both T1- and T2-weighted
3
images. On sagittal T2-weighted
images the identification of the
anatomic landmarks represented by
the displaced dura mater confirmed
the extradural nature of the collection
(Fig 1A). In normal conditions the
dura mater cannot be distinguished
from the adjacent spinal canal
on MRI. The administration of
contrast material demonstrated ring
enhancement typical of an organizing
abscess, which was essential in
confirming the infectious nature
of this collection (Fig 1B). In fact,
spontaneous extradural collections
may be indistinguishable from an
abscess based only on precontrast
images. Furthermore, the presence of
pathologic contrast enhancement in
the posterior aspect of the vertebral
body of C4 indicated the source of the
infection (Fig 1B). Early infectious
involvement of the spinal cord was
also noted (Fig 2).
Dr Horner
The anterior portion of the spinal
cord houses the anterior and
lateral spinothalamic tracts and
the anterolateral corticospinal
tracts. Therefore, compression of
this area, as noted on the MRI, may
cause loss of motor function below
the level of the injury and loss of
pain and temperature sensation
with preservation of fine touch
and proprioception.14 Given the
location in the cervical spine, there
is additional concern about loss of
respiratory drive because the phrenic
nerve arises from C3–5 roots.14
Dr Vellody, upon discovering these
results, did you have concern about a
potential change in his clinical status?
Dr Kishore Vellody (Pediatric
Hospitalist)
Yes, we certainly did. He looked
very well on examination despite
the impressive MRI spine findings.
However, the location of the abscess
indicated potential future neurologic
deficits. A cervical spinal cord
compression would be catastrophic
4
for this young infant, with potential
loss of his respiratory drive,
leading to complete cessation of
respiration. Additionally, there was
concern that the underlying support
structures and bones of the cervical
spine may also be compromised,
leading to greater instability in that
area. We immediately consulted
neurosurgeons for possible surgical
management of the abscess.
Concurrently, we arranged for
transfer to the pediatric ICU for
closer monitoring of his neurologic
status.
Dr Horner
The patient was transferred to our
pediatric ICU for monitoring. The
neurosurgeon was consulted for
evaluation of potential drainage of
the abscess.
Dr Greene, what is your
recommendation for medical or
surgical treatment of this case?
Dr Stephanie Greene (Pediatric
Neurosurgeon)
This child’s laboratory studies
raised concern about parameningeal
inflammation but not meningitis,
given the negative CSF culture. His
MRI findings are most consistent
with an epidural abscess. The
inflammation (and secondary
contrast enhancement) of the pia is
probably secondary to the abscess on
the outer side of the dura. Surgically
evacuating a ventral epidural abscess
would require an anterior cervical
approach. This space is extremely
small in infants, increasing the risk
of injury to the recurrent laryngeal
nerve (producing hoarseness and
swallowing dysfunction, which in
the worst case necessitates G-tube
placement) and esophagus. An
epidural abscess often produces a
phlegmon, such that an attempt to
evacuate it from a posterior approach
could result in no decompression or
microbiological specimen but rather
a wound to heal in the setting of
infection and the possible need for a
spinal fusion from a postlaminectomy
kyphosis in the future. The risks of
surgery greatly outweigh the benefits
in this neurologically intact infant.
To attempt to have interventional
radiology drain the abscess carries
additional risks of injury to the
vertebral artery on the side of
approach and possible introduction
of bacteria into the thecal sac.
Unfortunately, given the rarity of
cervical spinal abscesses in neonates,
the literature is inconclusive about
the necessity for surgical intervention
rather than antibiotics alone. There
are reports of cases managed with
surgical drainage15–19 but also with
antibiotics alone.20–22 Notably,
many of the case reports describing
surgical drainage of the abscess
involve patients with neurologic
compromise, whereas only 1 case
series described patients treated
with antibiotics alone who had
neurologic compromise.21 Expanding
to the pediatric population in general,
recent literature has demonstrated
appropriate recovery of children with
epidural abscess with antibiotics
alone, especially in those without
neurologic deficit.23–25 Given the
absence of neurologic compromise
in combination with the intradural
involvement (noted on MRI), we
thought empirical management with
antibiotics was preferable to the
sizable surgical risks.
Dr Horner
Dr Yamada, given the
recommendations by the
neurosurgeon, what is your approach
to medical treatment in this case?
Dr Masaki Yamada (Pediatric
Infectious Diseases)
Fortunately, the patient was
clinically stable, without persistent
bacteremia or neurologic symptoms
from cord compression at the time
of diagnosis. Therefore, we agreed
the risks outweighed the benefit,
and we mutually decided to manage
the abscess medically without
HORNER et al
Finally, STAT3 deficiency (hyper–
immunoglobulin E syndrome) has
been commonly associated with S.
aureus disease.28
FIGURE 3
A, The repeat sagittal T2-weighted image demonstrates near complete resolution of extradural
abscess (arrowhead). B, Minimal remaining enhancement in the vertebral body (arrow) and minimal
reactive dural enhancement (arrowhead) are seen on postcontrast T1-weighted images.
surgical intervention. After 14 days
of antibiotics, repeat spinal MRI
demonstrated a significant decrease
in size of the abscess (Fig 3). We
recommended a prolonged course
of 6 weeks of intravenous nafcillin
because there was no surgical
intervention.
Dr Horner
This patient was found to have an
extensive invasive infection with
MSSA involving bacteremia, vertebral
osteomyelitis, and epidural abscess at
a very young age.
Dr Rosenberg, should we be
concerned about an underlying
immunodeficiency, which may
increase his susceptibility to invasive
S aureus infections?
Dr Stacy Rosenberg (Pediatric
Allergy and Immunology)
It is important to consider an
underlying immunodeficiency
manifesting as a sentinel invasive
S. aureus infection, because several
immune deficiencies have increased
susceptibility to this particular
bacteria. Chronic granulomatous
disease (CGD) can present with
PEDIATRICS Volume 137, number 1, January 2016
invasive infections with catalasepositive organisms. Because CGD
is caused by mutations in the
nicotinamide adenine dinucleotide
phosphate oxidase complex, affected
people are susceptible to organisms
containing the enzyme catalase for
respiration using oxygen (catalase
positive), such as S aureus, Micrococci
species, Listeria monocytogenes,
Pseudomonas aeruginosa, and E coli,
as opposed to catalase-negative
organisms such as Streptococcus
and Enterococcus species. CGD is
diagnosed through evidence of
a defective phagocyte oxidative
burst.26 Abscesses can be found in
other disorders with phagocytic
defects, including leukocyte adhesion
deficiency and cyclic or congenital
neutropenia. Leukocyte adhesion
deficiency typically presents with
delayed umbilical cord separation
and a leukocytosis. Defects in
innate immunity, specifically tolllike receptor signaling, including
IRAK4 deficiency and MyD88
deficiency, are disorders with
increased susceptibility to S. aureus
infections and have a high risk of
mortality in the first decade of life.27
In our case, the patient’s young age
and invasive infection prompted an
immunologic workup to address
these potential underlying problems.
Ultimately, it was unrevealing. He
had normal neutrophil counts,
neutrophil oxidative burst
assay, toll-like receptor assay,
immunoglobulin G and M levels
(immunoglobulin A was probably
physiologically low), lymphocyte
proliferation, and severe combined
immunodeficiency newborn screen,
and he did not have lymphopenia.
He had many reassuring clinical
findings that were not suggestive
of an immunodeficiency, including
normal weight gain, development,
stooling pattern, and healing from
a circumcision and umbilical stump
separation. He lacked previous
rashes or infections and had a normal
physical examination with the
presence of tonsils.
FINAL DIAGNOSIS AND DISCUSSION:
MSSA BACTEREMIA, CERVICAL
VERTEBRAL OSTEOMYELITIS, AND
EPIDURAL ABSCESS
MSSA bacteremia is increasingly
being documented in the literature
and is a notable yet uncommon
pathogen in infants. In healthy,
febrile infants ≤90 days old with
bacteremia, only 5% have S. aureus
bacteremia.29 Neonates represent
7% to 31% of all children with
S. aureus bacteremia,30–33 with 1
additional pediatric study reporting
61% of S. aureus bacteremia
episodes occurring in neonates.34
S. aureus bacteremia occurs with
or without a source of infection.
For example, a source may be
the presence of a central venous
catheter, congenital heart disease
or endocarditis, musculoskeletal
infection, or CNS infection. Health
care–associated sources of S. aureus
5
bacteremia, specifically the rate of
its occurrence in the NICU given
the prevalence of central venous
catheters, is commonly described
in the literature.35,36 On the other
hand, S. aureus bacteremia without
a source is rare, and there is a
paucity of literature. A prospective
surveillance study demonstrated
that S. aureus bacteremia without a
source made up only 6% of the 631
S. aureus bacteremia events in the
series and occurred more often in
immunocompromised patients.33
More often, S. aureus bacteremia
occurs with a source, typically a
concomitant deep-seated infection,
which carries severe consequences if
left undiagnosed or undertreated.34,37
Thus, the diagnosis of a deep-seated
infection is integral to appropriate
treatment to decrease morbidity and
mortality. In the absence of central
venous catheters or congenital heart
disease, the most common sources
of S. aureus bacteremia are bone and
joint infections (11%–42%),30,31,38
endocarditis (0%–20%),30–32,34
and skin abscesses or cellulitis
(11%–56%).29–31,34,38 Less
commonly, deep-seated infections
occur in the musculoskeletal system
(pyomyositis), CNS (brain abscess,
epidural abscess, meningitis), and
lung (pneumonia).30,31,34,38 Studies
evaluating S. aureus bacteremia
demonstrate that deep-seated
infections are usually either clinically
apparent at presentation or occur in
children known to be at higher risk
secondary to the presence of central
venous catheters or congenital heart
disease.30,31,34,37,39 For instance,
the incidence of endocarditis in the
setting of S. aureus bacteremia ranges
from 0% to 20%, with a significantly
higher risk in those with congenital
heart disease, up to 50%.30–32,34,37
In fact, Valente et al32 showed that
9 out of 10 of their patients with S.
aureus bacteremia and infectious
endocarditis had congenital heart
disease.
6
The percentage of bacteremia in
children attributed to methicillinresistant S. aureus as opposed to
MSSA differs based on geographic
location and varies widely in
the limited existing literature,
ranging from 8% to 90% in NICU
patients34,35,40–42 and 6% to 33%
in non-NICU patients.30–34,38 Some
case series note methicillin-resistant
S. aureus to be more common
in health care–associated cases,
whereas others do not note this
difference.31–35,38,40–42
Vertebral osteomyelitis
complicated with an epidural
abscess is only occasionally seen in
immunocompetent children.23,43 The
majority are adolescents, with the
most common location of infection
being lower thoracic or lumbar
spines, as opposed to the cervical
spine in our patient. S. aureus is the
most common bacteria found in
epidural abscesses.23
Herein, we had a rare case of a
cervical vertebral osteomyelitis with
epidural abscess in an otherwise
healthy, immunocompetent infant.
The key points in making the
diagnosis were that S. aureus is not
a common pathogen for meningitis,
and the discrepancy between
the CSF analysis consistent with
bacterial meningitis and a sterile
CSF culture indicated parameningeal
inflammation. Both factors suggested
that additional evaluation to
identify a deep-seated infection was
warranted.
Our diagnostic steps were initially
focused on intracranial infection,
which was excluded with a head
computed tomography scan and
brain MRI with venography. Without
spinal MRI, the accurate diagnosis
could have been missed, which
demonstrates the importance of
thorough evaluation for a deepseated infection with S. aureus
bacteremia. Failure to diagnose the
vertebral osteomyelitis with epidural
abscess could have caused fatal
spinal cord injury.
A review of the literature reveals
2 other neonatal cases of vertebral
osteomyelitis and concomitant
epidural abscess but with different
bacterial organisms. One is a 3-weekold infant with fever noted to have
CSF pleocytosis with negative CSF
culture and Pasteurella multocida
bacteremia. He was treated
nonoperatively with intravenous
antibiotics without sequelae.20
The other is a 3-week-old infant
with fever, CSF pleocytosis, and
negative blood and CSF cultures;
however, the epidural abscess was
cultured, revealing β hemolytic
Streptococcus. This child underwent
operative drainage of the abscess and
recovered without sequelae.15
Worthy of special mention is that
these 2 infants and our patient all had
cervical osteomyelitis with adjacent
epidural abscess. Given this unusual
location, especially in this age group,
we postulated that perhaps cervical
injury with birth trauma or poor head
control may increase susceptibility
to bacterial infection in this location,
although this causal relationship
has not been proven previously, and
there was no history supportive of
birth trauma in any of the cases.
The standard therapy for epidural
abscesses is antibiotics and
surgical drainage, but conservative
nonoperative management with
antibiotics alone may be considered
in patients without neurologic deficit,
with extensive abscesses, or with
high surgical risks.23–25 Generally,
epidural abscesses do not always
warrant antibiotic treatment at
meningitic doses. However, we
continued the high dosing as if this
were bacterial meningitis because of
the initial CSF findings and concern
about potential spread of the
infection from the undrained abscess.
Given the anatomic complexity,
indications for surgical treatment
should be discussed for each case,
individually.
The patient uneventfully completed
6 weeks of intravenous nafcillin
HORNER et al
therapy and is doing well at 6 months
of age without neurodevelopmental
delay or other invasive infections at
all follow-up visits.
ABBREVIATIONS
CGD: chronic granulomatous
disease
CNS: central nervous system
CSF: cerebrospinal fluid
HSV: herpes simplex virus
MSSA: methicillin sensitive
Staphylococcus aureus
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