ABSCEDATION - keywords
abscedation
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abscedation: references
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Berman PH, Banker BQ (1966) Neonatal meningitis. A clinical and pathological study of 29 cases. Pediatrics 38:6–24.
de Vries LS, Verboon-Maciolek MA, Cowan FM, Groenendaal F (2006) The role of cranial ultrasound and magnetic resonance imaging in the diagnosis of infections of the central nervous system. Early Hum Dev 82(12):819-25.
Enzmann DR, Britt RH, Lyons B, Carroll B, Wilson DA, Buxton J (1982) High-resolution ultrasound evaluation of experimental brain abcess evolution: comparison with computed tomography and neuropathology. Radiology 142:95–102.
Gallagher PG, Ball WS (1991) Cerebral infarctions due to CNS infection with Enterobacter sakazakii. Pediatr Radiol 21:135–136.
Govaert P, de Vries LS (2010) Chapter 63; Bacterial meningitis, ventriculitis, 384. In: An Atlas of Neonatal Brain Sonography. Clinics in Developmental Medicine No.182-183. Mc Keith Press 2nd Ed.
Gray F, Alonso J-M (2002) Adams, J.H., Duchen, L.W. (Eds) Greenfield’s Neuropathology, seventh edition, London : Edward Arnold, ch 3, pp 151-190.
Larroche JC (1977) Developmental pathology of the neonate. Elsevier, Amsterdam. Chapter 23: bacterial meningo-encephalitis, p 462.
Licht-van der Stap RG, de Vries LS, Alarcon A, Govaert P, Steggerda SJ; EurUS.Brain group. Cranial ultrasound in neonatal brain infections. Dev Med Child Neurol. 2025 Aug;67(8):986-1003.Hung K-L (1986) Cranial ultrasound in the detection of post-meningitic complications in the neonates. Brain Dev 8:31–36.
Rennie JM, Hagmann CF, Robertson N (2008) The baby with a suspected infection. Chapter 13; 270. In: Neonatal Cerebral Investigation. Ed: Cambridge. ISBN-13 978-0-511-41368-1
Ries M, Deeg K-H, Heininger U, Stehr K (1993) Brain abscesses in neonates—report of three cases. Eur J Pediatr 152:745–746.
Veyrac C, Couture A, Baud C (1994) ‘La pathologie infectieuse.’ In: Couture, A., Veyrac, C., Baud, C. (Eds.) Echographie Cérébrale du Foetus au Nouveau-né. Montpellier: Sauramps Médical, pp. 371–382.
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typical images
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Abscess formation is a serious complication with a mortality of 15%. Most infants (75%) with an abscess present with meningitis. Outcome is generally poor, with learning disabilities in 70% and development of epilepsy in infancy or childhood in 60%. Abscess formation is associated with gram negative as well as positive bacteria and yeasts (Jaremko et al. 2011). Micro-abscesses in the subcortical-periventricular white matter and basal ganglia have been described in fungal meningitis as scattered, small, round hyperechoic lesions (Rennie et al. 2008). Citrobacter koseri but also Enterobacter sakazakii are especially likely to lead to abscess formation and the frontal or parietal lobe appear to be most often involved. Microabscesses coalesce into macroabscesses. Abscesses tend to be multiple (exception stafylococcus and aspergillus) and tend to coalesce.
With ultrasound first one sees a hyperechoic area without delineation (cerebritis). As central suppuration follows the centre may become less echoid (in some with a fluid level) and after about 6 days the margin towards grey matter becomes echoic and thicker, formation of the hyperechoic capsule. In the full blown stage there is a thick capsule, with central hypoechoic pus, but in some instances a hyperechoic nidus is seen in this centre (Veyrac and Couture 1994). This is when antibiotics may no longer reach the infection and drainage is mandatory. Contrast enhancement of the capsule is seen with MR techniques.
sequence
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bacillus cereus
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mature abscess with central pus (1), granulation (2), fibrous capsule (3) and glial reaction in adjacent brain tissue (4) (from Gray and Alonso 2002)
A brain abscess usually starts as a focal subcortical infarct caused by thrombophlebitis in white matter. Extension of a subependymal or cortical micro-infarction may also lead to abscess formation, in cerebrum and cerebellum. Entry of germs is often haematogenous, but local spreading is also possible in the newborn (via scalp infection, via infected emissary veins, via infected congenital fistulae). In the cortical grey itself abscesses are not readily formed. The abscess starts from cerebritis (white matter coagulation necrosis with inflammation and microthrombosis) that progresses to suppuration (Gray and Alonso 2002). The core of the area is relaced by pus while there is a gradual delination of the infected zone by collagen and reticulin, granulation tissue and neovascularisation. The encapsulation occurs mainly at the cortical face, in some cases pus clears via the ventricular face. An abscess will eventually be identified by a thick and irregular capsule, though in the neonatal period this is not always obvious (Enzmann et al. 1982, Gallagher and Ball 1991, Ries et al. 1993, de Vries et al. 2006). At the peak of cerebritis there may be a mass effect. About 10 to 14 days after the onset of ‘cerebritis’ the mass-effect, if any, disappears. It may be difficult to differentiate from a sterile postnecrotic cavity due to arterial infarction or haemorrhage. A late residual cavity can be integrated into the ventricle or becomes a glial nodule with calcification. An abscess rupturing through the arachnoidea can become a subdural empyema.
patterns
abscedation
abscedation: typical imaging
cerebellar abscess with stafylococcus aureus (two different preterm infants)(mastoidviews)
bacterial brain infection patterns
the sequence of events in neonatal bacterial brain infection
abscedation and cerebritis by bacillus cereus
New Text
preterm 19 days after birth, nosocomial infection with bacillus cereus: cerebritis and abscess formation in the left frontal lobe white matter
day 26: partial capsule formation and liquefaction necrosis in front of the abscess
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