Fever and Lethargy in an Infant
Radiology Cases in Pediatric Emergency Medicine
Volume 5, Case 8
Leo U. Pascua, MD
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
This is a 12-month old male in previously good
health presenting to a clinic with a history of fever for
two weeks (highest recorded temperature 39.1
degrees). The fevers were initially attributed to
teething. There is a dry, nonproductive cough for one
week. He has had a decreased appetite, but no
vomiting or diarrhea. Yesterday, he was noted to be
lethargic with decreased movement of his right arm and
left leg. His eyes would also roll. This morning, an aunt
came over to the home and found him to be quite
somnolent, poorly responsive and with abnormal
twisting movements of his extremities. This aunt
immediately brought him in to the nearest clinic.
Exam: T 37.3 (axillary), HR 165, RR 20, BP 143/93.
He is well developed and well nourished. He is tired
appearing, sometimes listless and somnolent. There is
no spontaneous movement of the entire right side of his
body. He has a modest left facial droop. Pupils are 5-6
mm bilaterally, sluggishly reactive to light, with
intermittent nystagmus. TM's unremarkable. His head
is turned to the left, with resistance felt when passively
rotating his head to the right (refuses to bring his chin to
the midline). Neck difficult to assess for rigidity. Heart
regular, no murmurs. Lungs clear. Abdomen benign,
scaphoid, no palpable masses, tenderness or
hepatosplenomegaly. Extremities slightly cool, pulses
somewhat diminished, but normal capillary refill time.
Skin clear. DTR's 2+ bilaterally. He holds his left leg
extended. His right hip is flaccid with the ipsilateral
knee in fixed flexion. With noxious stimuli, he does not
withdraw from pain at the right leg or right arm. His left
leg and left arm react normally. His plantar reflexes are
A CT of the brain is immediately ordered.
These two cuts from his CT scan series show
multiple 2-3 cm diameter loculated cystic lesions
consistent with multiple abscesses (dark areas with
rims of enhancement). There is distention of the
posterior fossa with a midline shift toward the right.
There is no sign of cribiform fracture or mastoiditis.
He is admitted to the intensive care unit where
infectious disease and neurosurgical consultations are
obtained. His initial work-up includes a CBC and
chemistry. A chest radiograph and an abdominal
radiograph are performed to look for signs of other
Admission labs: Na 141, K 3.4, Cl 99, bicarb 25,
gluc 127, Ca 10.3, phos 5.3, Alb 3, SGPT 8, SGOT 22,
BUN 10, creatinine 0.2. WBC 23.2 (49% segs, 14%
bands, 7% monos, 28% lymphs). Hgb/Hct 9/37.
Platelets 474,000. His chest radiograph is normal.
View abdominal flat plat.
An open safety pin is noted in his abdomen.
Shortly after admission, he developed seizures. He
was treated with anticonvulsants, cerebral dehydration
and controlled hyperventilation. Approximately 12 cc of
foul smelling, thick, yellow-green, purulent material was
needle aspirated through the lambdoidal suture. Gram
stain showed gram positive cocci in clusters, chains and
pairs. A burr hole was drilled into the right suboccipital
area, and a large posterior fossa abscess was aspirated
for yellow, creamy, opaque fluid. A left brain abscess
was visualized by ultrasound and needle aspirated for
85 cc of purulent material sent for culture. He was
initially started on ampicillin, clindamycin, and
gentamicin. His initial culture grew peptostreptococcus,
fusobacterium and alpha hemolytic streptococci, all of
which are oral bacteria. His antibiotics were changed to
vancomycin, ceftazidime, metronidazole, tobramycin,
Two days after admission, a follow-up abdominal
radiograph is obtained.
View follow-up abdominal film.
This abdominal film shows the safety pin to be
broken into two pieces now. It has not moved much.
There is residual barium in the bowel from a previous
contrast study which was unremarkable. Two weeks
later, the safety pin fragments are no longer seen.
An echocardiogram to rule out cardiac vegetations
showed a possible left atrial appendage lesion. A
repeat echo was normal, with no definite evidence of
left atrial mass.
His overall clinical progress was poor. Follow-up CT
scans showed recurrent abscesses and progressive
How the safety pin relates to his brain abscesses is
unclear. Cultures of the brain abscesses were not
positive for bowel organisms, but rather oral flora.
Perhaps the safety pin caused a perforation somewhere
in his pharynx or esophagus as it was going down.
The first reference to brain abscess was made by
Hippocrates in 460 B.C. Farre recognized brain
abscess as a complication of congenital heart disease
in 1840. The first operative treatment of brain abscess
was by Dupuytren in 1889.
Brain abscesses are the most frequent intracranial
suppurative process occurring in children, the
pathogenesis of which depends upon predisposing
conditions that also influence the anatomic location of
the abscess. The transmission of infection may occur
by continuity, as with penetration of the dura, or by
contiguity or juxtaposition. The membranous cranial
bones are formed from both dura and galea; therefore,
they derive their blood supply from both structures.
This intracranial/extracranial vascular connection
explains the mechanism for the development of cortical
thrombophlebitis. The diploic veins of Breschet are
valveless; therefore, blood may flow in either direction
and bacterial infection or septic emboli may gain access
intracranially. Cranial bone defects may occur and can
be either acquired or congenital. The posterior wall of
the frontal sinus, which is normally about one half the
thickness of the anterior wall, may be eroded by a
mucocele, infection, or neoplasm, or it may sustain
disruption due to trauma. The epidural space may
become infected in the dehiscent area, with abscess
formation and possibly secondary intracranial spread
throughout the dura.
Chronic otitis media, mastoiditis, meningitis and
congenital heart disease are the most common
predisposing factors, accounting for about 60% of brain
abscesses in children. Contiguous spread from ear,
nose or throat infections usually results in a single
abscess formed in proximity to the infected area, i.e.,
frontal abscess arising from ethmoid sinusitis, or
temporal or cerebellar abscess arising from mastoid
infection. The average age of these children is 5 to 10
years. Extension occurs via anastomosing veins.
Purulent material can also drain directly from an
infected sinus through the cribiform plate of the frontal
bone into the subdural space. Meningitis as a cause is
more common in children less than 2 years of age.
About 2% of children with cyanotic congenital heart
disease (i.e., right to left intracardiac shunts, pulmonary
arteriovenous fistulas) develop brain abscess.
Tetralogy of Fallot is the most common heart defect
leading to brain abscess formation. Infection is usually
with alpha-hemolytic streptococci. Organisms with a
predilection for hypercarbic/hypoxic areas have been
isolated. Mixed infections are uncommon.
Odontogenic (i.e., dental abscess), as well as
massateric space and infratemporal infections may be
the primary site. Head trauma (i.e., skull fracture), or
penetrating head injury are known risks for brain
abscess. P. multocida must be considered in a skull
penetrating dog bite. Ocular trauma (i.e., orbital roof or
temporal bone fracture) with wooden toys has been
associated with cerebral abscesses. In such cases
there is a male to female ratio of 3:1, with the most
common item being a graphite pencil. Wood, as a
penetrating agent carries a high risk of infectivity and
fragmentation. MRI may be needed to identify the
Abscess due to hematogenous spread (i.e., from
endocarditis, osteomyelitis, etc.), is usually along the
distribution of the middle cerebral artery in the posterior
frontal or parietal regions. Immunosuppressed patients
are also at risk. The presence of a ventroculoperitoneal
shunt increases the risk of infection by S. epidermidis
and S. aureus.
Citrobacter diversus or Proteus must be considered
in neonates with multiple brain abscesses. The
susceptibility of newborns to Gram-negative infection is
well established, and is explained by the deficiency of
both placentally transferred IgM antibodies and
complement. The physiological right to left shunt of the
neonatal blood circulation could explain the colonization
of the brain during septicemia.
No discernible underlying disease or source of
infection can be found in 30% of pediatric brain abscess
patients. In adults, pulmonary disease is the most
frequent cause for dissemination. This is not true for
Anatomic sites of infection are associated with
certain organisms. Frontal lobe abscesses (the most
frequent, 37%) are usually due to sinusitis, and usually
include aerobic and anaerobic streptococci, S. aureus,
S. pneumoniae, and H. flu. Cerebellar (2%) and
ipsilateral temporal lobe abscesses (11%) are usually
due to otitis media or mastoiditis. Common entities
include S. pneumoniae, H. flu, Enterobacter and B.
fragilis. Temporal, frontal and parietal lobe abscesses
(28%) have been associated with congenital heart
Multiple abscesses usually arise from meningitis,
pulmonary and VP shunt site infections, as well as
congenital heart disease. In the case of congenital
heart disease, abscesses usually arise along the
distribution of the middle cerebral artery. VP shunt
infections can involve S. aureus, S. epidermidis, Gram
negative enteric rods, and P. aeruginosa. Staph aureus
is the most common organism in brain abscesses due
to head trauma or surgical events. Enterobacter and
anaerobes can spread from intra-abdominal or
Focal areas of ischemia or necrosis (i.e., due to
suppurative vasculitis, hypoxic episode, embolism,
hyperviscosity, etc.) are a prerequisite for invasion by
microorganisms because the brain parenchyma is
resistant to infection. In addition to epidural or cerebral
abscess, the same mechanism applies to subdural
empyema as well as septic thrombophlebitis of the
emissary cortical veins or venous sinuses.
Four stages are recognized in the development of
brain abscesses. The first stage (early cerebritis) lasts
1-3 days, and is characterized by perivascular cuffing
with inflammatory cells in the region surrounding the
developing necrotic center, with marked cerebral
edema developing peripherally. During this cerebritic
stage (pre-encapsulation), antibiotics may still be able
to halt abscess development. The second stage (days
4 to 9) is characterized by early capsule formation via
fibroblasts, as well as neovascularization. The third
stage (days 10-13) shows definite capsule formation
with concomitant increase in fibroblast numbers, as well
as shrinkage of the necrotic center and diminishing
cerebritis. In the fourth stage (days 14 on), a well
defined necrotic center and a dense collagenous
capsule with peripheral cerebral edema can be seen.
The degree of symptomatology is a poor indicator of
whether the intracranial infection is still in the cerebritic
stage or has become encapsulated.
The most prominent clinical manifestations of brain
abscesses result from space-occupying effects in the
rigid cranial vault. Expansion of the lesion, bacterial
breakdown products, or macrophage induced cerebral
edema may result in increased intracranial pressure
and subsequent potentially lethal uncal or brainstem
herniation. The "classic" triad of fever, headache and
focal neurological deficits occurs in less than 50% of
patients (28% in one study; Saez-Llorens, 1989).
Seizures, and lethargy are common, as are hemicranial
headaches, alterations in consciousness, nausea, and
vomiting. Papilledema, ataxia and aphasia were also
reported. Sixth nerve palsy may indicate increased
intracranial pressure. Infants frequently present with
fever, meningismus, and/or a full fontanelle.
Symptoms can also depend upon the anatomic
sites, i.e., cerebellar abscess presenting with
nystagmus, ataxia, vomiting and dysmetria. The frontal
lobe is thought to be a neurologically silent area, and
thus abscess formation may not result in focal signs.
Subtle affective changes, behavioral problems, abusive
and profane language, depression, or euphoria may be
more indicative of changes in this area.
The differential diagnosis is extensive. Infectious
entities include viral encephalitis (especially herpes
simplex virus), subdural empyema, epidural abscess,
pyogenic meningitis, tuberculoma, cysticercosis,
echinococcosis, and cryptococcosis. Non-infectious
entities include primary and metastatic brain tumors,
subarachnoid or intracerebral hemorrhage, central
venous thrombosis, cerebral infarct, mycotic aneurysm,
chronic subdural hematoma, hemorrhagic
leukoencephalitis, or migraine.
Lumbar puncture is contraindicated due to the risk of
cerebral herniation. Cerebrospinal fluid is a poor source
for isolating the organism (positive cultures in only 7%;
Saez-Llorens, 1989), unless the abscess ruptures in to
the ventricular system, in which case the CSF WBC
count may be greater than 50,000 with a predominance
of polymorphonuclear cells. The CBC may reflect
peripheral leukocytosis with neutrophilia. Blood cultures
may be sterile. Electrolytes are generally normal,
unless hyponatremia suggests the development of
Between 1960 and 1974 the techniques used to
diagnose brain abscess included
pneumoencephalography, ventriculography, carotid
arteriography and nuclear brain scan. Since 1984, CT
of the brain has been the principal diagnostic technique.
Computed tomography remains the study of choice, as
it can discern the number, size and locations of
abscesses with a high degree of sensitivity and
specificity. A brain abscess usually appears as a
hypodense center with a surrounding ring which can be
contrast-enhanced. Other patterns include nodular
enhancement, and areas of low attenuation without
enhancement. The degree of enhancement is thought
to correlate with the degree of perivascular
inflammatory cell infiltration and neovascular
proliferation. Delayed films with an assessment of the
degree of enhancement in the center of the lesion may
differentiate between cerebritis (medical management
possible) and true encapsulated abscess (surgical
intervention more likely needed), the latter showing a
paucity of central contrast.
Skull films may show bubbles (pneumocephalus)
from gas-producing organisms within an abscess cavity
or outside the cranium. An electroencephalogram may
localize a focal lesion as opposed to a more generalized
lesion such a encephalitis. Seizure activity and diffuse
encephalopathic patterns have been reported. Low
frequency delta waves commonly signify a cerebral
abscess (slow wave foci). A brain scan should be
considered for patients with a negative CT if there is
still a strong suspicion of a brain abscess. Cerebral
arteriograms have demonstrated avascular masses.
The origin of the infection can dictate the choice of
initial antibiotic treatment. An initial trial of antibiotic
therapy may be warranted in patients who are
considered poor surgical candidates, have multiple
abscesses or abscesses in deep or difficult anatomical
locations, concomitant meningitis, or whose abscess
size is less than 4 cm or considered to be in the
Extensions of ENT infections can be treated with
penicillin (strep coverage, including S.milleri),
chloramphenicol (anaerobic coverage, high abscess
penetration), metronidazole (bactericidal for most
anaerobes, high abscess penetration, occasionally
achieving abscess concentrations greater than serum,
not degraded in purulent debris), or cefotaxime (active
against Hemophilus, Enterobacter, strep and staph).
Penetration is increased in infected tissue.
Nonetheless, penicillin-susceptible bacteria can be
cultured from abscesses for prolonged periods despite
antibiotic therapy. Inactivation of antibiotics may occur
by bacterial or leukocytic enzymes accumulating in the
purulent material trapped by the encapsulation,
subtherapeutic concentrations within the capsule, or
antagonism in the case of multiple antimicrobial agents.
Infection from head trauma or cranial surgery
warrants an antistaphylococcal agent, e.g. nafcillin.
Vancomycin is indicated when methicillin-resistant S.
aureus is prominent. With the exception of B. fragilis
and some other anaerobic strains, most of the
anaerobic pathogens are sensitive to penicillin.
Ampicillin is inadequate for empiric treatment because
of the increasing frequency of resistant E. coli and
Proteus spp., as well as unreliable penetration.
Aminoglycosides do not penetrate well into brain
abscesses, and they have reduced activity in the
anaerobic/acidic conditions associated with purulent
material. A beta lactamase-resistant penicillin, e.g.,
nafcillin, oxacillin or methicillin versus S. aureus, should
be added to metronidazole to cover aerobic and
Third generation cephalosporins are options for
treatment, given their efficacy against Gram negative
bacillary infection, broad coverage, high degree of
activity, and action against S. pneumoniae and H. flu.
Ceftazidime penetrates the subarachnoid space and is
active against P. aeruginosa. Older cephalosporins,
clindamycin and erythromycin have generally been
inadequate at achieving therapeutic concentrations.
Trimethoprim-sulfamethoxazole may cover aerobic
Gram-positive and Gram-negative rods.
Chloramphenicol may be bactericidal against S.
pneumoniae, Hemophilus spp. and most of the obligate
anaerobes including B. fragilis, but bacteriostatic
against S. aureus and Enterobacter. Direct instillation
of antibiotics in the abscess cavity during aspiration has
been reported, but efficacy of this technique has not
been formally assessed.
Corticosteroid use is controversial. It is thought to
retard the encapsulation process, as well as decrease
endothelial permeability of vessels associated with the
inflammatory reaction, and thereby reduce the amount
of brain water. However, it may increase necrosis,
reduce antibiotic penetration into the abscess, and alter
CT scan images of ring enhancement. Steroid therapy
can also produce a rebound effect when discontinued.
Thus, corticosteroid use to reduce cerebral edema
should be as short a course a possible.
The duration of treatment depends upon the
patient's clinical response, imaging findings,
organisms isolated, and the extent and type of surgical
drainage, if any. For those patients undergoing
excision, 7 to 10 days for parenteral therapy has been
suggested. Three to four weeks are probably required
for patients treated with aspiration, and a minimum of 4
weeks for those treated with antibiotics alone.
Debate continues as to whether excision of the
abscess wall is preferable to single or multiple
aspirations of the cavity. The latter appears to be
preferred in children, on the basis of comparable
mortality rate and of less potential damage to the brain
tissue from surgical trauma. Aspiration is used for brain
abscess in early infancy, in large abscesses with poor
capsule formation and in most centrally or deeply
located abscesses. Stereotaxic aspiration or aspiration
guided by operative neurosonography is performed in
deep hemispheric abscesses or multiple abscesses
with an intracranial mass effect. If the patient has
increasing neurologic deficit, including deteriorating
consciousness or signs of increasing intracranial
pressure, surgery is necessary.
The predominant mode of surgical therapy was
craniotomy with abscess resection. Intraoperatively, it
is important to prevent ventricular or leptomeningeal
contamination. Biopsy of brain tissue may be
necessary if mucormycosis or neoplasm is suspected.
The mortality rate of brain abscess varies in the
literature from 11 to 53%, and is increased with
increased duration of symptoms before medical
intervention, coma on admission, young age, larger
abscess size, multiple abscess, and rupture into the
cerebral ventricles or subarachnoid space.
Improvements include the use of CT scanning,
improved methods for isolating anaerobic flora, and
more effective antimicrobial treatment. Morbidity is
increased in patients who undergo aspiration, rather
than evacuation or resection.
Neurological sequelae (seizure disorders,
hemiparesis, optic atrophy, spasticity, cranial nerve
palsy, hydrocephalus, behavior disorder, school
learning disabilities) can be present in up to 60% of
patients. Conversely, complete recovery has been
reported in 40% of patients. The incidence of
neurologic sequelae has been lower when abscesses
were aspirated (facilitated greatly by CT) rather than
Serial CT scans are the mainstay of clinical
follow-up, especially after antibiotics therapy is
discontinued. A suggested regimen for serial CT's is
every 2-4 weeks until resolution of the lesion, then at
2-4 month intervals for 1 year. Successful therapy
would be indicated by a progressive decrease in the
degree of ring enhancement, edema, mass effect, and
size of the lesion.
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