Pyogenic Brain Abscess

= focal area of necrosis beginning in area of cerebritis with formation of surrounding membrane

Prevalence: 0.4–0.9÷100,000

Cause:

1. Extension from paranasal sinus infection (41%) / mastoiditis / otitis media (5%) / facial soft-tissue infection / dental abscess
2. Generalized septicemia (32%):
   1. lung (most common): bronchiectasis, empyema, lung abscess, bronchopleural fistula, pneumonia
   2. heart (less common): CHD with R-L shunt (in children >60%), AVM, bacterial endocarditis
   3. osteomyelitis
3. Penetrating trauma or surgery
4. Cryptogenic (25%)

Predisposed: diabetes mellitus, patients on steroids / immunosuppressive drugs, congenital / acquired immunologic deficiency

Organism: anaerobic streptococcus (most common), bacteroides, staphylococcus; in 20% multiple organisms; in 25% sterile contents

Pathophysiologic stages:

1. Early cerebritis = vascular congestion, petechial hemorrhage, edema ← neutrophilic response to invasive organism
   • ill-defined hypoattenuation on NECT
   • absent / variable enhancement on CECT
2. Late cerebritis = cerebral softening + necrosis ← marginal fibroblast accumulation (but NO collagen deposition) ← breakdown of blood-brain barrier
   • ringlike enhancement diffusing centrally on delayed images
   • suppressed enhancement after corticosteroid Rx
     Capsule develops over 2–4 weeks = SIGNATURE imaging feature of an abscess!
3. Early capsule = fibroblasts create reticulin matrix ← blockage of necrotic material
4. Late capsule = matrix transitions to mature collagen
   Histo: liquefaction + cavitation + capsule + pericapsular (progressively decreasing) edema
   • Capsule:
     1. inner layer of granulation tissue
     2. middle layer of collagen
     3. outer layer of astroglia
   • well-vascularized capsule tends not to persist on delayed scan
   • NO suppressed enhancement after corticosteroid Rx
   • capsule often thinner medially ← relatively poor vascularity + reduced fibroblast migration
     Cx:
     1. daughter abscesses
     2. intraventricular rupture

• headache, drowsiness, confusion, seizure
• focal neurologic deficit
• fever, leukocytosis (resolves with encapsulation)

Location: typically at corticomedullary junction; frontal and temporal lobes; supratentorial÷infratentorial = 2÷1

NECT:

• well-defined hyperattenuated ring compared with central necrosis + peripheral edema:
• zone of low density with mass effect (92%)
• slightly increased rim density (4%) ← development of collagen layer takes 10–14 days
• gas within lesion (4%) is diagnostic of gas-forming organism

CECT:

• ring enhancement (90%) with peripheral zone of edema
• continuous regular smooth 2–7-mm ring, nonspecific but HIGHLY CHARACTERISTIC of a pyogenic abscess!
• homogeneous enhancement in lesions <0.5 cm
• edema + contrast enhancement suppressed by steroids
• multiloculation + subjacent daughter abscess in white matter

MR: (most sensitive modality)

• abscess centrally increased / variable intensity on T2WI
• T1-hyperintense + T2-hypointense rim (= abscess capsule) ← paramagnetic effect of bactericidal free radicals generated by active macrophages
• outside border of increased SI on T2WI (edema)
• restricted diffusion in abscess core ← high cellularity and viscosity of pus impedes water mobility
  • (CHARACTERISTIC) hyperintensity on DWI
  • corresponding hypointensity on ADC maps
  
  DWI is the best sequence for differentiation of ring-enhancing pyogenic abscess from necrotic tumor.

MR spectroscopy:

• ↑amino acid level (0.9 ppm) = marker of proteolytic enzymes from neutrophils (in 80%)

Cx:

1. Development of daughter abscesses toward white matter
2. Rupture into ventricular system / subarachnoid space (thinner capsule formation on medial wall of abscess related to relative hypovascularity) → ventriculitis ± meningitis

Dx helpful features:

• multiple lesions at gray-white matter border
• clinical history of altered immune status
• R-to-L shunt: eg, pulmonary AV fistula
• foreign travel
• high-risk behavior: eg, IV drug abuse

Rx: IV antibiotics (penetrate brain abscess to therapeutic levels) + needle aspiration for best clinical outcome

DDx:

1. Primary / metastatic neoplasm (restricted diffusion typically in tumor periphery ← high cellular density
2. Subacute infarction
3. Resolving hematoma