Sonography of neonatal intracranial infection

Summary: Meningoencephalitis occurs in 25% of newborns with bacterial sepsis due to entrance of bacteria into the central nervous system via the choroid plexus of the lateral ventricle. Structural brain damage from inflammation, edema, and vasculitis may be demonstrated sonographically in young infants, even in the absence of neurological findings. Sonographic findings include increased echogenicity of cortical sulci, widening of the sulcal echoes, and extraaxial fluid collections (due to accumulation of an inflammatory exudate within the sulci and fissures that may result in extraaxial fluid collections); slit-like ventricles initially with diffuse increased parenchymal echogenicity (due to diffuse brain edema and inflammation) or mild to moderate ventricular dilatation (resulting from arachnoiditis, which interferes with cerebrospinal fluid resorption); ventriculitis (manifested by ventricular enlargement, echogenic cerebrospinal fluid secondary to inflammatory cells and debris, and intraventricular septations or bands from glial proliferation that may compartmentalize and cause obstructive hydrocephalus); meningoencephalitis (associated with focal or diffuse, unilateral or bilateral, abnormal parenchymal echogenicity secondary to edema, cerebritis, and/or infarction); abscess formation (well-circumscribed lesions with a thick echogenic wall developing within an echogenic area of cerebritis or infarction); or multicystic encephalomalacia (end-stage result of meningoencephalitis with cerebral necrosis due to vasculitis and hypoxia). Dystrophic calcification is most often associated with cytomegalovirus (CMV), toxoplasmosis, and herpes simplex virus.