A combination of vasogenic and cytotoxic edema arises from many infectious processes within the central nervous system. Other forms of edema may also occur in infections, including hydrocephalic edema secondary to CSF obstruction and osmotic
edema due to SIADH. Numerous infectious agents have direct toxic effects generating vasogenic edema through alteration of the BBB and cytotoxic edema from endotoxin-mediated cellular injury. Bacterial wall products stimulate the release of various endo-thelial factors, resulting in excessive vascular permeability. This injurious effect is augmented by a hyperemic response within the first 24-48 hr that elevates ICP to precarious levels. Associated immu-nologic and inflammatory responses can also engender cerebral edema. Cerebral edema is a critical determinant of morbidity and mortality in pediatric meningitis. Abscess formation or focal invasion of the brain results in an isolated site of infection surrounded by a perimeter of edema encroaching on the neighboring parenchyma. This ring of vasogenic and cytotoxic edema may produce more symptoms than the actual focus of infection. Similar regions of focal or diffuse edema may accompany encephalitis, particularly viral infections such as herpes simplex encephalitis.
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