Evidence map›Paper›PMID 25304462›Full record

ArticlePediatric radiology2014

Neonatal deep white matter venous infarction and liquefaction: a pseudo-abscess lesion.

Lynne Ruess, Carly M Dent, Hailey J Tiarks, Michelle A Yoshida, Jerome A Rusin

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Article in Pediatric radiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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5 authors at 1 institution in 1 country.

Lynne RuessDepartment of Radiology, Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH, 43205, USA, lynne.ruess@nationwidechildrens.org.
Carly M Dent
Hailey J Tiarks
Michelle A Yoshida
Jerome A Rusin
Nationwide Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDeep white matter hemorrhagic venous infarction with subsequent cavitation due to necrosis and liquefaction has been described in neonates and may be associated with infection and meningitis. In our experience, the MRI pattern of these lesions is confused with the pattern seen with cerebral abscesses.

objectiveThe purpose of our study was to characterize the MRI findings of post infarction necrosis and liquefaction after hemorrhagic deep white matter venous infarction in infants and to distinguish these lesions from cerebral abscesses. MATERIALS AND

methodsAn institutional review board approved a retrospective review of imaging records to identify all patients with cerebral venous infarction at a children's hospital during a 10-year period. Nine infants had deep white matter hemorrhagic venous infarction with white matter fluid signal cavitary lesions. A diagnosis of cerebral abscess was considered in all. The imaging and laboratory findings in these patients are reviewed and compared to descriptions of abscesses found in the literature.

resultsThere were six female and three male infants. The mean age at presentation was 20 days (range: 0-90 days), while the corrected age at presentation was less than 30 days for all patients. Seven patients presented with seizures and signs of infection; one infant presented with lethargy and later proved to have protein C deficiency. MRI was performed 0-12 days from presentation in these eight patients. Another patient with known protein C deficiency underwent MRI at 30 days for follow-up of screening US abnormalities. There were a total of 38 deep cerebral white matter fluid signal cavitary lesions: 25 frontal, 9 parietal, 2 temporal, 2 occipital. Larger lesions had dependent debris. All lesions had associated hemorrhage and many lesions had evidence of adjacent small vessel venous thrombosis. Lesions imaged after gadolinium showed peripheral enhancement. Three lesions increased in size on follow-up imaging. Three patients, two with meningitis confirmed via microbiology and one with presumed meningitis by CSF counts, underwent surgical aspiration of a total of six lesions. All specimens were sent for pathology and culture and were negative for microorganisms.

conclusionRecognizing the MR appearance of cavitary necrosis and liquefaction after deep white matter cerebral venous infarction in neonates can distinguish this entity from cerebral abscess and potentially avoid an unnecessary neurosurgical aspiration procedure.

Indexed as

Brain AbscessBrain InfarctionCerebral HemorrhageHumansInfantInfant, NewbornMagnetic Resonance ImagingMaleReproducibility of ResultsSensitivity and SpecificityWhite Matter

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PMID25304462
OpenAlexW1989269923

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