BRAIN ABSCESS

Epidemiology
• Approximately 1500–2500 cases per year in the U.S. Incidence is higher in developing countries.
• Male: female ratio is 1.5–3:1.
Risk factors
Risk factors include pulmonary abnormalities (infection, AV-fistulas…, see below), congenital cyanotic heart
disease (see below), bacterial endocarditis, penetrating head trauma (see below), chronic sinusitis or otitis
media, and immunocompromised host (transplant recipients on immunosuppressant, RA, RF, leukemia , DM,
HIV/AIDS).
Vectors
• Prior to 1980, the most common source of cerebral abscess was from contiguous spread.
Now, hematogenous
• Dissemination is the most common vector. In 10–60% no source can be identified

Hematogenous spread
The chest is the most common origin:
1. Arteriovenous fistulas pulmonary : ≈ 50% of these patients have Osler-Weber-Rendu syndrome (AKA
hereditary hemorrhagic telangectasia), and in up to 5% of these patients a cerebral abscess will eventually
develop.
2. Bacterial endocarditis: only rarely gives rise to brain abscess. More likely to be associated with acute
endocarditis than with subacute form.
3. congenital cyanotic heart disease (CCHD) in children (estimated risk of abscess is 4–7%, which is≈ 10-
fold increase over general population), especially tetralogy of Fallot (which accounts for ≈ 50% of cases). The
increased Hct and low PO2 in these patients provides an hypoxic environment suitable for abscess
proliferation.
Those with right-to-left (veno-atrial) shunts additionally lose the filtering effects of the lungs (the brain seems
to be a preferential target for these infections over other organs). Streptococcal oral flora is frequent, and may
follow dental procedures.
Coexisting coagulation defects often further complicate management
4. Dental abscess
5. Empyema lung abscess (the most common in adults), bronchiectasis.
6. Famale pt pelvic infections may gain access to the brain via Batson’s plexus.
7.GI infections

Contiguous spread
1. osteomyelitis of sinuses caused by purulent sinusitis: spreads osteomyelitis local or by phlebitis of emissary
veins. Virtually always singular. Rare in infants because they lack aerated paranasal and mastoid air cells.)
ethmoidal and frontal sinusitis → frontal lobe abscess.
sphenoid sinusitis: the least common location for sinusitis, but with a high incidence of intracranial
complications due to venous extension to the adjacent cavernous sinus → temporal lobe.
2. odontogenic → frontal lobe. Rare. Associated with a dental procedure in the past 4 weeks in most cases.also
spread hematogenously.

Dr: Zuhair Abughareb 1 Edited by: Hager Aldhubhani

3. otitis media and mastoiditis middle-ear and mastoid air sinus infections → temporal lobe and cerebellar
abscess. The risk of developing a cerebral abscess in an adult with active chronic otitis media is ≈ 1/10,000
per year (this risk appears low, but in a 30-year-old with active chronic otitis media the lifetime risk becomes
≈ 1 in 200).

Following penetrating cranial trauma or neurosurgical procedure

▪ Following penetrating trauma: The risk of abscess formation following civilian gunshot wounds tothe
brain is probably very low with the use of prophylactic antibiotics, except in cases with CSF leak not
repaired surgically following traversal of an air sinus.
▪ An abscess following penetrating trauma cannot be treated by simple aspiration as with other abscesses;
open surgical debridement to remove foreign matter and devitalized tissue is required.
▪ Post-neurosurgical: especially with traversal of an air sinus.
▪ Abscess has been reported following use of intracranial pressure monitors and halo traction
Pathogens
1. Cultures from cerebral abscesses are sterile in up to 25% of cases
2. Organisms recovered varies with the primary source of infection
3. In general: streptococcus is the most frequent organism; 33–50% are anaerobic or microaerophilic.
Multiple organisms may be cultured to varying degrees (depends on care of technique), usually in only 10–
30% of cases, but can approach 60%,17 and usually includes anaerobes (Bacteroides sp. common)
4. when secondary to fronto-ethmoidal sinusitis: Strep. milleri and Strep. anginosus may be seen
5. from otitis media, mastoiditis, or lung abscess: usually multiple organisms, including anaerobic strep.,
Bacteroides, Enterobacteriaceae (Proteus)
6. posttraumatic: usually due to S. aureus or Enterobacteriaceae
7. odontogenic (dental) source: may be associated with Actinomyces
8. following neurosurgical procedures: Staph. epidermidis and aureus may be seen
9. immunocompromised hosts, including transplant patients (both bone marrow and solid organ) and AIDS:
fungal infections are more common than otherwise would be seen. Organisms include:
a) Toxoplasma gondii
b) Nocardia asteroides
c) Candida albicans
d) Listeria monocytogenes
e) mycobacterium
f) Aspergillus fumigatus often from a primary pulmonary infection
10. infants: Gram-negatives are common because IgM fraction of antibodies don’t cross the placenta
Presentation
▪ Adults: no findings are specific for abscess, and many are due to edema surrounding the lesion. Most
symptoms are due to increased ICP (H/A, N/V, lethargy). Hemiparesis and seizures develop in 30– 50%
of cases. Symptoms tend to progress more rapidly than with neoplasms.
▪ Newborns: patent sutures and poor ability of infant brain to ward off infection → cranial enlargement.
▪ Papilledema is rare before 2 yrs of age

Dr: Zuhair Abughareb 2 Edited by: Hager Aldhubhani

Histologic staging of cerebral abscess
Stage Histologic characteristics
1- early cerebritis: (days 1–3) early infection & inflammation, poorly demarcated from surrounding brain,
toxic changes in neurons, perivascular infiltrates, intermediate resistance, hypointense in T1.
2- late cerebritis: (days 4–9) reticular matrix (collagen precursor) & developing necrotic center, no resistance.
3- early capsule: (days 10–13) neovascularity, necrotic center, reticular network surrounds (less well
developed along side-facing ventricles), no resistance.
4- late capsule: (> day 14) collagen capsulea, necrotic center, gliosis around capsule firm resistance, “pop” on
entering abscess is ≈ the only process in the brain that leaves a collagen scar; all other scars are glial scars.
Evaluation
Bloodwork
▪ Peripheral WBC: may be normal or only mildly elevated in 60–70% of cases (usually > 10,000).
▪ Blood cultures: should be obtained when abscess is suspected, usually negative.
▪ ESR: may be normal (especially in congenital cyanotic heart disease CCHD where polycythemia lowers
the ESR).
▪ C-reactive protein (CRP): hepatic synthesis increases with inflammatory conditions; however, infection
anywhere in body (including brain abscess and dental abscess) can raise the CRP level. May also be
elevated in noninfectious inflammatory conditions and brain tumor.
Sensitivity for abscess is≈ 90%, specificity is ≈ 77%.
Brain imaging
▪ CT
▪ Ring enhancing. Sensitivity ≈ 100%. For CT staging of abscess
▪ MRI
▪ Enhanced T1WI → thin-walled ring enhancement surrounding low intensity central region Fluid-fluid
levels may be seen. Occasionally gas-producing organisms may cause pneumocephalus.
▪ Diffusion MRI: DWI → bright, ADC → dark (restricted diffusion suggesting viscous fluid)
Unlike most tumors which are dark on DWI More reliable with pyogenic abscess, less reliable e.g., with
fungal or TB abscess).
▪ MR-spectroscopy: presence of amino acids and either acetate or lactate are diagnostic for abscess.
Additional evaluation
▪ CXR and chest CT (if indicated) to look for pulmonary source.
▪ Cardiac echo (including TEE, Doppler and/or echo with agitated saline injection (bubble study): for
suspected hematogenous spread, to look for patent foramen ovale or cardiac vegetations
Treatment
There is no single best method for treating a brain abscess. Treatment usually involves:
● Cutoff more than 3cm Surgical treatment: needle drainage or excision
● Correction of the primary source
● Conservative management long-term use of antibiotics: often IV x 6–8 weeks and possibly followed by oral
route x 4–8 weeks. Duration should be guided by clinical and radiographic response.
Indications for surgical treatment
1. Mass effect exerted by lesion (on CT or MRI).
2. Approached to ventricle: indicates likelihood of intraventricular rupture which is associated with poor
outcome, difficulty in diagnosis (especially in adults).
3. Size by 4 wks no decrease with antibiotic.
4. Severe neurologic condition (patient responds only to pain, or does not even respond to pain).
5. Evidence of significantly increased intracranial pressure
6. Fungal abscess
7. Follow-up CT/MRI scans cannot be obtained every 1–2 weeks

Dr: Zuhair Abughareb 3 Edited by: Hager Aldhubhani

8. Conservative management failure : neurological deterioration, progression of abscess towards ventricles,
or after 2 wks if the abscess is enlarge.
9. Encapsulations is multiloculated
10. Traumatic abscess associated with foreign material

Indications for Medical

1. Less than cutoff: small diameter of abscesses successfully treated with antibiotics alone.
2. Duration of symptoms ≤ 2 wks (correlates with higher incidence of cerebritis stage).
3. Improvement clinical within the first week.
4. Clotting disorders poor surgical candidate (NB: with local anesthesia, stereotactic biopsy can be done in
almost any patient with normal blood coltting).
5. Multiple abscesses, especially if small.
6. Abscess in poorly accessible location: e.g.,brainstem.
7. Ependymitis meningitis concomitant.

Management
• Send blood cultures
• Start antibiotic therapy (preferably after biopsy specimen is obtained), regardless of which mode of
treatment (medical vs. Surgical) is chosen
• LP: avoid in most cases of cerebral abscess
• Seizure medications: indicated for seizures, prophylactic use is optional
• Steroids: controversial. Reduces edema, but may impede therapy (see below)

Antibiotic selection
1. Initial antibiotics of choice when pathogen is unknown, and especially if S. aureus is suspected (if there is
no history of trauma or neurosurgical procedure, then the risk of MRSA is low):
● Vancomycin: covers MRSA. 15 mg/kg IV q 8–12 hours to achieve trough 15–20 mg/dl PLUS
● A 3rd generation cephalosporin (ceftriaxone); utilize cefepime if post surgical
PLUS
● metronidazole (Flagyl®). Adult: 500mg q 6–8 hours
● Alternative to cefepime + metronidazole: meropenem 2 g IV q 8 hours
● Make appropriate changes as sensitivities become available
2. If culture shows only strep, may use PCN G (high dose) alone or with ceftriaxone
3. If cultures show methicillin-sensitive staph aureus and the patient does not have a beta lactam allergy, can
change vancomycin to nafcillin (adult: 2 g IV q 4 hrs. peds: 25 mg/kg IV q 6 hrs)
4. Cryptococcus neoformans, Aspergillus sp., Candida sp.: Liposomal amphotericin B 3–4 mg/kg IV daily +
flucytosine 25 mg/kg PO QID.
5. In AIDS patients: Toxoplasma gondii is a common pathogen, and initial empiric treatment with
sulfadiazine + pyrimethamine + leucovorin is often used 6. for suspected or confirmed nocardia asteroides,

Antibiotic duration
• IV antibiotics for 6–8 wks (most commonly 6), NB: CT improvement may lag behind clinical
improvement. Duration of
• Treatment may be reduced if abscess and capsule entirely are excised surgically. Oral antibiotics may
be used following IV course.

Dr: Zuhair Abughareb 4 Edited by: Hager Aldhubhani

Follow-up imaging
If therapy is successful, imaging should show decrease in:
1. edema
2. degree of ring enhancement
3. mass effect
4. Extent of lesion : takes 1 to 4 wks
SURGERY
1. Needle aspiration: the mainstay of surgical treatment. Especially well-suited for
• Deep
• Elder pt
• Elecoent area
• Poly lesions ,may also be used with thin-walled or immature lesions
2. Surgical excision: Shortens length of time on antibiotics and reduces risk of recrudescence. Recommended
in traumatic abscess to debride foreign material (especially bone), and in fungal abscess because of relative
antibiotic resistance
Outcome
In the pre-CT era, mortality ranged from 40–60%. With advances in antibiotics, surgery, and the improved
ability to diagnose and follow response with CT and/or MRI, mortality rate has been reduced to ≈ 10%, but
morbidity remains high with permanent neurologic deficit or seizures in up to 50% of cases.
A worse prognosis is associated with
• Poor neurologic function,
• Intraventricular rupture of abscess,
• Fungal abscesses
• Transplant recipients.

Dr: Zuhair Abughareb 5 Edited by: Hager Aldhubhani