Brain Abscess

Dr. Mahesh ChaudharyResident Phase BMD Radiology & Imaging BSM Medical University, Dhaka

Introduction Abscess is initiated by focal intracranial

infection as an area of cerebritis and evolves into a collection of pus surrounded by a vascularized capsule.

Most common in first four decades of life

Males are more commonly affected

Infants and neonates its rare (may occur as complication of bacterial meningitis)

Causative agents (1/3rd mixed)

Adults : Streptococci, Staphylococci Gram-negative (Escherichia coli, Klebsiella, Proteus, Pseudomonas, H. influenzae)

Neonates and children : Citrobacter, Proteus, Pseudomonas, Serratia and Staphyloccocus aureus

Mostly the causative agents are bacteria but there can be fungal or granulomatous or Parasitic agents

In 20-30% of abscesses, cultures are sterile and no specific organism is identified.

Causes of brain abscess Hematogenous

dissemination Cyanotic heart disease Cardiac(infective endocarditis) Drug abuse Pulmonary infection Sepsis Urinary tract infection Congenital or acquired dural dehiscence

Direct extension Otitis Paranasal sinus Mastoditis Calvarial or meningeal infection

Trauma Penetrating injury Postsurgical No predisposing factors in 25% of cases

Location

Corticomedullary(gray-white junction) most common location Frontal and parietal lobes are most frequent sites

Subdural space Temporal lobe and cerebellum (OM & mastoiditis)

15% posterior cranial fossa Multiple uncommon except in immunocompermised

PresentationMost Common Headache most common symptom (up to 90%);Fever in approximately 50%

Other signs: Seizures, altered mental status, focal neurologic deficitsIncreased erythrocyte sedimentation rate (ESR)(75%), elevated WBC count (50%)CSF study- increase protein & increase white cell count

Pathology: four stages of evolution Early cerebritis (3-5 days) Infection is focal but not localized Unencapsulated mass of PMNs, with edema Scattered foci of necrosis and petechial hemorrhage

Late cerebritis (4-5 days up to 2 weeks) Necrotic foci coalesce Rim of inflammatory cells, macrophages, granulation tissue,

fibroblasts surrounds central necrotic core Vascular proliferation, surrounding vasogenic edema

There is a focal unencapsulated mass of petechial hemorrhage, inflammatory cells, and edema

Autopsy case demonstrates typical pathologic findings of late cerebritis with significant mass effect, edema. The coalescing lesion shows some central necrosis and an illdefined rim of petechial hemorrhage .

Pathology: 4 stages of evolution Early capsule (begins at around 2 weeks) Well-delineated collagenous capsule Liquefied necrotic core, peripheral gliosis

Late capsule (weeks to months) characteristic 3 layers1. An inner inflammatory layer of granulation tissue &

macrophages2. A middle collagenous layer 3. An outer gliotic layer

Autopsy case shows typical findings of a cerebral abscess at the early capsule stage. The liquefied necrotic core of the lesion is surrounded by a well-developed capsule

Autopsy case shows late capsular stage with well delineated collagenous core that surrounds the necrotic core.

Daughter lesion is also seen

Imaging modalities

CT MRI DWI MRS NUCLEAR MEDICINE STUDIES

COMPUTED TOMOGRAPHY (NECT) Early cerebritis: Ill-defined hypodense subcortical lesion with mass effect May be normal early Late cerebritis: Central low density area; peripheral edema, Mass effect increase Early capsule: Hypodense mass with moderate vasogenic edema & mass effect Thin well delineated capsule Late capsule: Edema, mass effect diminish

COMPUTED TOMOGRAPHY (CECT) Early cerebritis: +/- Mild patchy enhancement

Late cerebritis: Irregular peripheral rim enhancement

Early capsule: Low density center with thin distinct enhancing capsule

Deep part of capsule is thinnest(near ventricle); thickest near cortex

Late capsule: Cavity shrinks, capsule thickens May be multiloculated and have "daughter"abscesses

MRI T1WI Early cerebritis: Poorly marginated, mixed hypointense/isointense

mass

Late cerebritis: Hypointense center, isointense/mildly hyperintense rim,

edema present nearly always

Early capsule: Thick irregular rim; isointense to hyperintense to white matter; center hyperintense to CSF

Late capsule: Cavity shrinks, capsule thickens

MRI T2WI

Early cerebritis: Ill-defined hyperintense mass

Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema

Early capsule: Hypointense rim ; Related to collagen, hemorrhage, or paramagnetic free radicals

Late capsule: Edema and mass effect diminish

MRI Tl C+ Early cerebritis: Patchy enhancement

Late cerebritis: Intense but irregular rim enhancement

Early capsule: Well-defined, thin-walled enhancing rim

Late capsule: Cavity collapses, thickened enhancement of capsule Capsule is thinnest on the ventricular side

DWI, MRS AND NUCLEAR MEDICINE STUDIES

DWI : Increased signal intensity in cerebritis and abscess

ADC map: Markedly decreased signal centrally within abscess

MRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate, pyruvate, and amino acids

Nuclear Medicine Findings PET: FDG and Carbon-ll-Methionine have shown increased uptake in

brain abscess

Resolving abscess• Hyperintense on T2WI, FLAIR; hypointense rim resolves• Small ring/punctate enhancing focus may persist for months

Complication of Brain Abscess • Formation of satellite lesions• Ventriculitis• Choroid plexitis• Purulent leptomeningitis

A tiny ill defined enhancing focus is present in left frontal lobe

9 days later pre and post contrast axial scan MRI shows a predominantly low signal left frontal mass with irregularly enhancing rim , edema and mass effect.

5 weeks after drainage and antibiotic therapy axial CECT scans shows a small ring enhancing residual left frontal lobe mass. Some edema persists but is diminished. This is the late capsule stage of abscess formation. Enlarged ventricle with persistent choroid plexitis.

Abscess caused by gas-forming organism. Gas is seen with a surrounding low-density area on noncontrast CT scan. Contrast CT scan shows irregular, ring like enhancement; gas is visible within the cavity. The causative organism was Escherichia coli

Mature abscess: T2-weighted image shows a mature abscess with hypointense rim, central cavity, and adjacent surrounding edema. A small satellite lesion is also seen. Gadolinium-enhanced MRI study demonstrates smooth, ring like enhancement corresponding to thehypo intense rim seen on T2-weighted images.

Treatment

Surgical drainage and/or excision primary therapy

Antibiotics only, if small « 2.5 cm) or early phase of cerebritis

Steroids to treat edema and mass effect

Lumbar puncture hazardous, pathogen often can't be determined from CSF

Differential diagnosis Tuberculoma

Tuberculoma

The second most common manifestation of neurotuberculosis Parenchymal infection with central caseating necrosis Secondary to pulmonary TB rarely GI or GU tract. Occurs at any age; most commonly in first three decades

Location : Cerebral hemispheres(frontal and parietal & basal ganglia Less commonly brainstem and dura

Pathology

Non caseating with solid center or caseating with necrotic center

Rarely progresses to TB abscess Lobulated mass with thick rim in parenchyma subarachnoid

space or dura Size: range from 1mm to 6cm

Clinical presentation Seizures, increased intracranial pressure, papilledema

Imaging NECT Hypodense to hyperdense round or lobulated nodule/mass with moderate to marked edema.

CECT Solid or ring enhancing Target sign : central calcification or enhancement followed by enhancing rim

MRI T1WI: Non caseating granuloma: Hypointense to brainCaseating granuloma with solid/necrotic center: Hypointense or isointense

Caseating granuloma may have hyperintense rim

T2WI: Noncaseating granuloma: Hyperintense to brain Caseating granuloma with solid center: Iso- to hypointense with hypointense

rim Caseating granuloma with necrotic center: Central hyperintensity with

hypointense rim Hypointense rim + surrounding edema common

FLAIR Similar to T2 characteristics

TI C+Noncaseating granuloma: Nodular, homogeneous enhancementCaseating granuloma with solid center: Peripheral rim enhancementCaseating granuloma with necrotic center: Peripheral rim-enhancement, central low signal

MRA: vessel narrowing, irregularity, occlusion MRS : prominent lipid, lactate but no amino acid resonances

Two small lesions with thick ring enhancement

T2WI shows multifocal tuberculomas as hypointense foci surrounded by edema

T1C+ scan in the same case illustrates additional lesions with punctate , ring enhancement

Thank You