Dr. Schor of the National Institute of Neurological Disorders and Stroke has no relevant financial relationships to disclose.)
Literature focused on the physiologic mechanisms of cerebral edema in the pediatric population is limited and often extrapolated from the adult population; however, there are many hypotheses on the mechanisms of brain edema for this defined population. In this article, the author provides a synoptic description of pathophysiologic mechanisms of cerebral edema in the pediatric patient. The author describes cytogenic and vasogenic mechanisms of brain edema in patients with Reye syndrome, Reye-like syndrome, toxic exposure, neuroexcitatory encephalopathy, viral encephalopathy, fulminant hepatic failure, shaken baby syndrome, and diabetic ketoacidosis. New information further elucidating the etiology and underlying mechanisms of cerebral edema in children with severe diabetic ketoacidosis is presented in this update.
Historical note and terminology
Pediatric researchers continue to struggle to understand important differences in how the developing brain responds to a variety of insults as compared to the mature organism. Among other factors, Kochanek speculates that the developing brain might have a greater predisposition to set the apoptotic cascade into motion after injury (Kochanek 2006).
Brain edema manifests clinically as encephalopathy although it may be defined on the basis of specific pathologic and radiographic findings. Pediatric cerebral edema has many different characteristics that can be difficult to delineate categorically, as many patients follow a progressive clinical course with pathophysiologic aspects of both vasogenic and cytotoxic injury. This article describes the more commonly identified causes of cerebral edema affecting the pediatric population.
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