ALG Brain Abscess
of the major dural venous sinuses and corti-
BASIC INFORMATION
DEFINITION
A brain abscess is a focal intracerebral infection
that can arise as a complication from a bacte-
rial, mycobacterial, fungal, or parasitic infection,
surgery, or trauma.
ICD-10CM CODES
G06.0 Intracranial abscess and granuloma
EPIDEMIOLOGY &
DEMOGRAPHICS
INCIDENCE: Uncommon (reported incidence 0.4
to 0.9 cases per 100,000 population; occurs
about 2% as commonly as brain tumors)
PEAK INCIDENCE: Preadolescence and middle
age (and depends on predisposing condition);
increased rates in the immunocompromised host
PREDOMINANT AGE: Occurs at any age
PREDOMINANT SEX:
• Men affected more than women (ratio 2:1 to
3:1)
PHYSICAL FINDINGS & CLINICAL
PRESENTATION
• Classic triad: fever, headache, and focal
neurologic deficit (present in less than 50%
of cases).
• Clinical presentation is often due to the
manifestations of the space-occupying lesion
rather than to signs of systemic infection.
• Fever is present in only 32% to 79% of
patients.
• Headache is usually localized to the side of
the abscess; onset can be gradual or severe;
present in an average of 70% to 75% of cases.
• Focal neurologic findings (e.g., seizures,
hemiparesis, aphasia, ataxia) depend on the
location of the abscess and are seen in 23%
to 66% of cases.
• Papilledema is present in 9% to 51% of cases.
• Presence of adjacent infections (dental
abscess, otitis media, sinusitis, or postneu-
rosurgical infection) may be a clue to the
underlying diagnosis and should be sought in
any suspected case.
• Time course from symptom onset to presen-
tation ranges from hours in fulminant cases
to more than 1 month; 75% present in the
first 2 weeks.
• The nonspecific presentation of a brain
abscess warrants that clinicians maintain a
high index of suspicion. Table 1 describes
common initial features of brain abscess.
ETIOLOGY
• Brain abscesses are classified based on the
likely portal of entry and can arise from:
Contiguous infection (e.g., dental abscess,
otitis media, sinusitis, or post neurosurgi-
cal infection)
Hematogenous spread from a remote site
(e.g., endocarditis, bacteremia)
• Likely source of abscess and common organ-
isms involved:
A. Contiguous focus or primary infection
(55% of all brain abscesses):
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207
TABLE 1  Brain Abscess: Initial
Features in 123 Cases
Headache 55%
Disturbed consciousness 48%
Fever 58%
Nuchal rigidity 29%
Nausea, vomiting 32%
Seizures 19%
Visual disturbance 15%
Dysarthria 20%
Hemiparesis 48%
Sepsis 17%
From Goldman L, Schafer AI: Goldman’s Cecil medicine, ed 24,
Philadelphia, 2012, Saunders.
1. Paranasal sinus: occur in frontal
lobe; streptococci (especially micro-
aerophilic and anaerobic strepto-
cocci), Bacteroides, Haemophilus, and
Fusobacterium spp.
2. Otitis media/mastoiditis: occur in
temporal lobe and cerebellum; aer-
obic and anaerobic streptococci,
Enterobacteriaceae, Bacteroides, and
Pseudomonas spp.
3. Dental sepsis: occur in frontal lobe;
mixed Fusobacterium, Bacteroides, and
Streptococcus spp. (especially S. viri-
dans and anaerobic streptococci)
4. Penetrating head injury: site of abscess
depends on site of wound; Staphylococcus
aureus, aerobic streptococci, Clostridium
spp., Enterobacteriaceae
5. Postoperative: Staphylococcus epider-
midis and S. aureus, Enterobacteriaceae,
and Pseudomonas aeruginosa
B. Hematogenous spread from a distant site
of infection (25% of all brain abscess-
es): abscesses most commonly multiple,
especially in middle cerebral artery dis-
tribution; infecting organism(s) depend on
source.
1. Congenital heart disease: streptococci,
Haemophilus spp.
2. Endocarditis: S. aureus, viridans strep-
tococci
3. Urinary tract: Enterobacteriaceae,
Pseudomonadaceae
4. Intraabdominal: streptococci,
Enterobacteriaceae, anaerobes
5. Lung: streptococci, Actinomyces spp.,
Fusobacterium spp.
6. Immunocompromised host: Toxoplasma
spp., Enterobacteriaceae, Nocardia spp.,
listeriosis, other fungi, tuberculosis
a. Fungi are responsible for up to
90% of cerebral abscesses in solid
organ transplant recipients.
C. Cryptogenic (unknown source): 20% of
all brain abscesses
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
• Other parameningeal infections: subdural
empyema, epidural abscess, thrombophlebitis
cal veins
• Embolic strokes in patients with bacterial
B
endocarditis
• Mycotic aneurysms with leakage
• Acute hemorrhagic leukoencephalitis
• Parasitic infections: toxoplasmosis, echino-
coccosis, cysticercosis
• Metastatic or primary brain tumors
• Cerebral infarction
• CNS vasculitis
• Chronic subdural hematoma
and Disorders
Diseases
WORKUP
Physical examination, laboratory tests, and
imaging studies
LABORATORY TESTS
• White blood cell counts are elevated in 60%
of patients. I
• Erythrocyte sedimentation rate is usually
elevated but may be normal.
• L umbar puncture is contraindicated
because of the potential for increased
intracranial pressure and the risk for herni-
ation due to the space-occupying abscess.
Lumbar puncture may be helpful only in
those with suspicion for meningitis or
abscess rupture into the ventricular sys-
tem; however, the risk of herniation must
be considered.
• The yield of gram stain and culture of mate-
rial aspirated at time of surgical drainage is
very high.
• Cultures of contiguous sites of infection
should be considered (e.g., paranasal sinus,
otitis, skin site abscess from a neurosurgi-
cal procedure). These sites of infection may
need surgical drainage in order to control the
infection.
• Blood cultures and cerebrospinal fluid cul-
tures may identify the causative organism in
up to 25% of patients.
IMAGING STUDIES
• CT scan with contrast enhancement or MRI
with gadolinium can be used to detect brain
abscess. CT is rapid and available in most
medical settings. An MRI with gadolinium is
able to provide more detailed images in order
to differentiate between abscess and tumor
or other mass.
• CT scan (Fig. 1) with intravenous contrast
enhancement is still an excellent test (sensi-
tivity 95%-99%).
• Serial CT or MRI scanning is recommended to
follow the response to therapy.
TREATMENT
ACUTE GENERAL Rx
• Effective treatment involves a combination of
empiric antibiotic therapy and timely excision
or aspiration of the abscess.
• If evidence of edema or mass effect, treat-
ment of elevated intracranial pressure is
paramount.
• Hyperventilation of mechanically venti-
lated patient.
208 Brain Abscess ALG

• Dexamethasone initially in a dosage of
10 mg IV followed by 4 mg IV q6h until
symptoms of cerebral edema subside.
Steroids should be discontinued as soon
as possible.
• Mannitol 0.25 to 1 g/kg IV over 20 to 30
min q6 to 8h; maximum of 6 g/kg in 24 hr.
• Medical therapy is never a substitute for
surgical intervention to relieve increased
intracranial pressure. Neurologic deteriora-
tion usually mandates surgical intervention.
• Steroids should be limited to patients with
severe cerebral edema or midline shift.
MEDICAL Rx
If abscess <2.5 cm and patient is neurologically
stable and conscious, may start antibiotics and
observe. Empiric antibiotic therapy guided by:
• Abscess location
• Suspicion of primary source
• Presence of single or multiple abscesses
• Patient’s underlying medical conditions (e.g.,
HIV, immunocompromised)
Selection of empiric antibiotic therapy:
• Primary infection or contiguous source:
1. Otitis media/mastoiditis, sinusitis: third-
generation cephalosporin (cefotaxime 2
g q4h IV or ceftriaxone 2 g q12h IV) plus
metronidazole 15 mg/kg IV as a loading
dose, then 7.5 mg/kg q8h IV, not to exceed
4 g per day
2. Dental infection: penicillin G (20 million to
24 million units per day IV in six divided
doses) plus metronidazole (dose as above)
3. Head trauma: third- or fourth-generation
cephalosporin (cefotaxime 2 g IV q4h or
ceftriaxone 2 g IV q12h or cefepime 2 g IV
q8h) plus vancomycin (30 mg/kg IV in two
divided doses adjusted for renal function)
4. Postoperative neurosurgery: vancomycin
(dose as above) plus ceftazidime (2 g
surrounding region
of hypodensity from
vasogenic edema parietal
lesion
IV q8h) or cefepime (2 g IV q8h), or
meropenem (1 g IV q8h). Replace vanco-
mycin with nafcillin (2g IV q4h) if suscep-
tibility testing reveals methicillin-sensitive
Staphylococcus aureus.
• Hematogenous spread (congenital heart
disease, endocarditis, urinary tract, lung,
intraabdominal): vancomycin (empiric thera-
py, dose as above) or nafcillin (if susceptibility
testing reveals methicillin-sensitive S. aure-
us, dose as above) plus metronidazole plus
third-generation cephalosporin (cefotaxime 2
g IV q4h or ceftriaxone 2 g IV q12h). Antibiotic
therapy can be adjusted based on the etiol-
ogy of the underlying infection, if known.
• HIV infected or immunocompromised patient:
metronidazole plus a third-generation cepha-
losporin, antifungal, or antiparasitic agent
Duration of antibiotic therapy is guided by the
clinical course and by whether the abscess was
surgically aspirated or excised; it is usually pro-
longed. Most recommend parenteral treatment
for at least 4 to 8 weeks, with serial neuroim-
aging to ensure adequate resolution. (Imaging
weekly could be considered for first 2 weeks
of therapy, then every 2 weeks until resolution.)
Surgical therapy may be required for clinical
failure (i.e., increasing size of abscess on imag-
ing despite antibiotic therapy).
SURGICAL Rx
• Three indications for surgical intervention:
1. Collect specimens for culture and
s­ensitivity
2. Reduce mass effect
3. Clinical failure with antibiotic therapy
alone
• Stereotactic biopsy or aspirate of the abscess
if surgically feasible
• Essential to selection of targeted antimicro-
bial coverage
surrounding
region of
hypodensity
(darker gray)
from
vasogenic
edema
• Timing and choice of surgery depends on:
• Primary infection source
• Number and location of the abscesses
• Whether the procedure is diagnostic or
therapeutic
• Neurologic status of the patient
DISPOSITION
• Prompt diagnostic consideration, early insti-
tution of appropriate antimicrobial thera-
py, and advanced neuroradiologic imaging
have reduced the mortality rate from brain
abscesses from 40% to 80% in the preanti-
biotic era to 10% to 20% at present.
• Morbidity is usually manifest as persistent
neurologic sequelae (seizures, intellectual or
behavioral impairment, motor deficits).
REFERRAL
Consultation with a neurosurgeon is mandatory.
PEARLS &
CONSIDERATIONS
COMMENTS
• It is important to maintain a high index of
suspicion because a brain abscess often
presents with nonspecific symptoms.
• Rapid imaging and early institution of appro-
priate antimicrobial therapy improve patient
morbidity and mortality.
• Neurosurgical consultation is mandatory.
PREVENTION
Because brain abscesses arise from either
contiguous infections or hematogenously from a
remote site, early and appropriate treatment of
predisposing infections is paramount to prevent
brain abscess.
SUGGESTED READINGS
Available at www.expertconsult.com
RELATED CONTENT
Brain Abscess (Patient Information)
AUTHOR: ERICA HARDY, M.D., M.M.S.

lesion
enhances
with IV
A B contrast

FIG. 1  Brain abscess.  This 48-year-old male presented with status epilepticus. Computed tomography (CT)
of the brain showed a parietal mass, which at brain biopsy was found to be an abscess. Cultures grew mixed
gram-positive and gram-negative organisms and anaerobes. The patient was subsequently found to be human
immunodeficiency virus positive. A, Noncontrast head CT, brain windows. B, CT with intravenous (IV) contrast
moments later, brain windows. Abscesses and other infectious, inflammatory, or neoplastic lesions typically
have surrounding hypodense regions representing vasogenic edema. When IV contrast is administered (B), the
lesion may enhance peripherally, often referred to as ring enhancement. (From Broder JS: Diagnostic imaging
for the emergency physician, Philadelphia, 2011, Saunders.)

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Brain Abscess 208.e1

SUGGESTED READINGS
Brouwer MC, Tunkel AR, McKhann GM, van de Beek D: Brain abscess, N Engl J
Med 371:447–456, 2014.
Helweg-Larsen J, Astradsson A, Richhall H, et al.: Pyogenic brain abscess – a 15
year survey, BMC Infectious Diseases 12:332, 2012.
McClelland 3rd S, Hall WA: Postoperative central nervous system infections: inci-
dence and associated factors in 2111 neurosurgical procedures, Clin Infect
Dis 45:1, 2007.

Downloaded for Matdoan Rifkiah Aisyah (matdoan.rifkiah@ui.ac.id) at Universitas Indonesia from ClinicalKey.com by Elsevier on May 12, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.