Brain Abscess The early stages of cerebritis and abscess formation are associated with

nonspecific symptoms, including low-grade fever, headache, and lethargy. As

the inflammatory process proceeds, vomiting, severe headache, seizures,
Brain abscesses can occur in children of any age but are most common in
papilledema, focal neurologic signs (hemiparesis), and coma may develop. A
children between 4 and 8 yr old and in neonates. The causes of brain abscess
cerebellar abscess is characterized by nystagmus, ipsilateral ataxia and
include embolization as a result of congenital heart disease with right-to-left
dysmetria, vomiting, and headache. If the abscess ruptures into the ventricular
shunts, endocarditis, meningitis, chronic otitis media and mastoiditis, sinusitis,
cavity, overwhelming shock and death usually ensue.
soft-tissue infection of the face or scalp, orbital cellulitis, dental infections,
severe complicated pneumonia, penetrating head injuries, immunodeficiency
When the brain parenchyma is infected, the first manifestation is a focal
states, and infection of ventriculoperitoneal shunts.
cerebritis with surrounding edema, which is then encapsulated over days to
weeks by inflammatory granulation tissue surrounding the core of necrotic
Abscesses are focal infections consisting of encapsulated pus and pyogenic
tissue. Where in the brain an abscess develops generally depends on the source
bacteria, or, less commonly, mycobacteria, fungi, or protozoa. Abscesses of the
of infection: sinusitis, especially frontal, and infections of the oral cavity tend to
central nervous system may be found in the brain parenchyma itself, as well as
cause frontal lobe abscesses, and otitis media and mastoiditis lead to abscesses
in the intracranial epidural space and spinal epidural space.
in the parietal/temporal region.
Predisposing factors are found in most (∼80%) of cases of brain abscess;
Fever is present in 50% of patients with a brain abscess, and a history of
approximately 20% of abscesses in modern case series are idiopathic. Among
headaches is even more common, in 60% to 70%. Although older patients may
cases with predisposing factors, 30% to 50% stem from a contiguous focus of
localize their headaches toward the site of the abscess (right or left side, front or
infection (eg, otitis media, mastoiditis, sinusitis, or orbital cellulitis);
back of the head), young children usually cannot. Approximately half of all
approximately 30% are associated with bacteremia (eg, cyanotic congenital
patients have focal neurologic findings, and approximately 25% have seizures.
heart disease, pulmonary disease, or odontogenic infection); approximately 10%
result from disruption of the body’s natural barriers (eg, neurosurgical
The classic clinical triad suggestive of brain abscess—fever, headache, and focal
procedure or head trauma); and approximately 10% occur in the presence of an
neurologic findings—is more specific than sensitive, as only 20% of affected
immunosuppressive condition (eg, solid organ transplant or leukemia).
patients exhibit all 3 at diagnosis. If the abscess has been present for long
enough or is big enough to significantly increase intracranial pressure,
Pathology
papilledema may be found on examination; this is in contrast to bacterial
meningitis, which presents too quickly for papilledema to develop
Cerebral abscesses are evenly distributed between the 2 hemispheres, and 80%
of cases are divided equally between the frontal, parietal, and temporal lobes.
Brain abscesses in the occipital lobe, cerebellum, and brainstem account for
approximately 20% of the cases. Most brain abscesses are single, but 30% are
multiple and may involve more than 1 lobe. An abscess in the frontal lobe is
often caused by extension from sinusitis or orbital cellulitis, whereas abscesses
located in the temporal lobe or cerebellum are frequently associated with
chronic otitis media and mastoiditis.

Etiology

A BA can develop from three sources: First because of spread of infection from
pericranial contiguous focus in 25-50% of cases (such as the sinuses, middle
ear, or dental infection), interestingly dental infections, ethmoid or frontal
sinusitis (usually spreads to the frontal lobe), and subacute or chronic otitis
media or mastoiditis (preferentially spreads to the inferior temporal lobe and
cerebellum).
Differential Diagnoses
The second from is hematogenous spread from a distant focus of infection
[such as lung abscess or empyema, bacterial endocarditis, skin infections, and • Bacterial meningitis
intra-abdominal (including pelvic)] in 15-30% of cases. In some of the patients • Brain cancer (primary or metastatic)
with cryptogenic BA, it can be possible to find a cardiac source, a congenital • Cryptococcosis
heart disease, like a patent foramen ovale (PFO) or a pulmonary arteriovenous • Cysticercosis
fistula,PFO is a primary contributory factor to BA by permitting infected material • Epidural Abscess
to bypass the lungs and enter the systemic circulation. Third, from direct • Focal encephalitis
inoculation (such as head trauma or neurosurgery) in 8-19% of cases. • Mycotic aneurysm
• Septic cerebral emboli causing infarction
The predominant organisms causing brain abscesses in children are aerobic and • Septic dural sinus thrombosis
anaerobic streptococci (60-70% of the cases) with Streptococcus milleri gp
(Streptococcus anginosus, Streptococcus constellatus, and Streptococcus Stages of Brain Abscess
intermedius) being increasingly isolated from surgically drained brain abscesses.
Other important streptococci include group A and B streptococci, Streptococcus
pneumoniae, and Enterococcus faecalis. Other bacteria isolated from brain
abscesses include anaerobic organisms (Gram-positive cocci, Bacteroides spp.,
Fusobacterium spp., Prevotella spp., Actinomyces spp.) and Gram-negative
aerobic bacilli (Haemophilus aphrophilus, Haemophilus parainfluenzae,
Haemophilus influenzae, Enterobacter, Escherichia coli, Proteus spp.).
Diagnosis
Citrobacter is most common in neonates.
The peripheral white blood cell count can be normal or elevated, and the blood
In contrast, the most common causative organisms in patients with head
culture is positive in 10% of cases. Examination of the cerebrospinal fluid shows
trauma or neurosurgical procedures are Staphylococcus aureus, coagulase-
variable results; the white blood cells and protein may be minimally elevated
negative staphylococci, or gram-negative bacilli. Very rarely, organisms such as
or normal, and the glucose level may be low. Cerebrospinal fluid cultures are
Actinomyces species, Nocardia species, Mycobacterium tuberculosis, Candida
rarely positive; culture of pus from the neurosurgical drainage is the key to
species, Aspergillus species, or Toxoplasma gondii may cause brain abscesses,
establishing a bacteriologic diagnosis. Because examination of the
especially in immunocompromised children. At least 25% of brain abscesses
cerebrospinal fluid is seldom useful and a lumbar puncture may cause
yield polymicrobial growth in culture, an important consideration in treatment
herniation of the cerebellar tonsils, the procedure should not be undertaken in a
decisions.
child suspected of having a brain abscess. The electroencephalogram shows
corresponding focal slowing, and the radionuclide brain scan indicates an area
Somewhat surprisingly, bacterial meningitis in children and adults is very rarely
of enhancement caused by disruption of the blood–brain barrier in more than
associated with brain abscess, despite the intense inflammation and bacterial
80% of cases. CT with contrast and MRI are the most reliable methods of
load in the meninges covering the brain.
demonstrating cerebritis and abscess formation. MRI is the diagnostic test of
choice. The CT findings of cerebritis are characterized by a parenchymal low-
density lesion, and MRI T2-weighted images indicate increased signal intensity.
An abscess cavity shows a ring-enhancing lesion by contrast CT, and the MRI
also demonstrates an abscess capsule with gadolinium administration.

Whereas the child with possible or probable acute bacterial meningitis requires
prompt lumbar puncture for diagnosis, the most important initial study for
diagnosis of brain abscess is cranial imaging, with either MRI or computed
tomographic (CT) scanning with intravenous (IV) contrast. A hypodense lesion
Clinical Manifestations on CT scanning is consistent with the cerebritis of a newly forming abscess, and
focal edema on MRI suggests the presence of a mass lesion. As an abscess
matures, IV contrast yields a classic ring-enhancing image with a necrotic
center and surrounding edema. Diffusion-weighted MRI can distinguish brain
abscesses from other cerebral masses with diagnostic sensitivity and specificity
greater than 95% by showing a homogenous, hyperintense signal with
corresponding hypointense signal on the apparent diffusion coefficient
sequence.
Again, unlike the situation with suspected meningitis, a lumbar puncture should
not be performed when brain abscess is a serious consideration because of the
risk of herniation from elevated intracranial pressure and because CSF is not
likely to identify the infecting pathogen. In a meta-analysis of patients with brain
abscess who did have a lumbar puncture because of uncertainty of diagnosis,
only 25% had a positive CSF culture, but 7% had clinical deterioration attributed
to the procedure. Identification of the causative organism is best attempted by
obtaining Gram-stain and culture information on material obtained through
stereotactic aspiration of the abscess. Blood cultures may identify the causative
organism in one-third of cases. If culture is negative but bacterial abscess is
strongly suspected, performing a polymerase chain reaction amplification of
bacterial 16S ribosomal DNA sequences may be able to detect bacterial DNA;
however, such testing is not yet standardized or routinely available.
therapy. Corticosteroids are sometimes used to reduce brain edema in
symptomatic patients, but at the risk of reducing antimicrobial penetration. ]
The main complications of brain abscess are hydrocephalus from direct
compression by a posterior fossa abscess and ventriculitis from rupture of an
abscess into the ventricular system, which carries a 27% to 85% mortality rate.
Other complications include increased intracranial pressure, brain herniation,
and status epilepticus. The case fatality rate of brain abscess has declined
substantially in the past 6 decades with improvements in cranial imaging,
neurosurgical techniques, and antimicrobial therapy.
Prognosis
Factors associated with high mortality rate at the time of admission include age
younger than 1 yr, multiple abscesses and coma. Long-term sequelae occur in
about one-third of the survivors and include hemiparesis, seizures,
hydrocephalus, cranial nerve abnormalities, and behavior and learning
problems.

Treatment

The initial management of a brain abscess includes prompt diagnosis and

institution of an antibiotic regimen that is based on the probable pathogenesis
and the most likely organism. When the cause is unknown, the combination of
vancomycin, a third-generation cephalosporin, and metronidazole is
commonly used. If there is a history of penetrating head injury, head trauma, or
neurosurgery, vancomycin plus a third-generation cephalosporin is
appropriate. When cyanotic congenital heart disease is the predisposing factor,
ampicillin-sulbactam alone or a third-generation cephalosporin plus
metronidazole may be used. Meropenem has good activity against Gram-
negative bacilli, anaerobes, staphylococci, and streptococci, including most
antibiotic-resistant pneumococci, and may be used alone to replace the
combination of metronidazole and a β-lactam in the previous regimens.
Abscesses secondary to an infected ventriculoperitoneal shunt may be initially
treated with vancomycin and ceftazidime. When Citrobacter meningitis (often in
neonates) leads to abscess formation, a third-generation cephalosporin is used,
typically in combination with an aminoglycoside. Listeria monocytogenes may
cause a brain abscess in the neonate and if suspected, ampicillin should be
added to the cephalosporin.

A brain abscess can be treated with antibiotics without surgery if the abscess is
<2 cm in diameter, the illness is of short duration (<2 wk), there are no signs of
increased intracranial pressure, and the child is neurologically intact. If the
decision is made to treat with antibiotics alone, the child should have follow-up
neuroimaging studies to ensure the abscess is decreasing in size. An
encapsulated abscess, particularly if the lesion is causing a mass effect or
increased intracranial pressure, should be treated with a combination of
antibiotics and aspiration. Surgery is indicated when the abscess is >2.5 cm in
diameter, gas is present in the abscess, the lesion is multiloculated, the lesion
is located in the posterior fossa, or a fungus is identified. The duration of
antibiotic therapy depends on the organism and response to treatment but is
usually 4-6 wk.

Management of brain abscess may require multidisciplinary input of critical

care, neurosurgical, neurologic, and infectious diseases experts. Associated
lesions may require consultants in otorhinolaryngology and ophthalmology as
well.

Neurosurgical intervention is generally undertaken in most patients with brain

abscesses, both for etiologic diagnosis and reduction of lesion size. Stereotactic
aspiration via a burr hole is now the most common procedure, rather than
craniotomy. Excision of the entire abscess itself is performed in approximately
25% of patients, especially in those with abscesses larger than 2.5 cm or in
cases of symptomatic cerebral edema or ventricular rupture. In stable patients
with multiple abscesses, none of which are greater than 2.5 cm in diameter,
nonsurgical management with antibiotic therapy has had success in some
reports.

Intravenous antimicrobial therapy should be given without delay to patients

with a brain abscess; antibiotic therapy should be deferred only if aspiration or
surgery can be accomplished in the next few hours. The empirical choice of
agent(s) should depend on the most likely organism(s). Thus, for cases likely to
have spread from the middle ear, sinuses, or orbits, a third-generation
cephalosporin (cefotaxime or ceftriaxone) plus metronidazole is appropriate
(with the addition of vancomycin if methicillin-resistant S aureus is suspected).
An alternative regimen suggested by some experts is meropenem with or
without metronidazole. If head trauma or a neurosurgical procedure is thought
to be a factor, vancomycin plus metronidazole, plus a third- or fourth-
generation (cefepime) cephalosporin is indicated. In children who are
immunosuppressed, therapy may need to be directed against Nocardia
(trimethoprim-sulfamethoxazole), Aspergillus or other fungi (voriconazole), or
Toxoplasma (pyrimethamine-sulfadiazine).

The duration of IV antibiotic therapy is typically 6 to 8 weeks, sometimes

followed by a course of an oral agent such as amoxicillin–clavulanic acid or
metronidazole. The success of therapy should be monitored with serial CT scans
or MRIs; imaging should confirm significant improvement at the end of planned