Dissociation of cerebral blood flow, glucose metabolism, and electrical activity in pediatric brain death

Abstract

A 2-month-old infant demonstrated clinical brain death 48 hours after suffering a closed head injury accompanied by cardiac arrest. Two nuclear cerebral blood flow (CBF) studies demonstrated normal perfusion. On the 11th day following injury, cerebral electrical activity ceased and a normal glucose metabolic gradient between gray and white matter was documented on positron emission tomography. Autopsy revealed widespread necrosis with mononuclear cell infiltrates throughout all cerebral cortical layers. Nine children have previously been described with clinical brain death, electrocerebral silence, and evidence of CBF by radionuclide scan. The dissociation between cerebral electrical activity and blood flow may be explained by an increase in cranial volume allowed by the expansile neonatal skull, preventing both intracranial hypertension and a reduction in perfusion pressure. The persistence of glucose metabolism may be associated with the presence of inflammatory microglial cells in the ischemic cortex. The authors conclude that persistence of CBF and glucose metabolism in brain-dead children may not indicate neuronal survival. If repeated neurological examinations with or without electroencephalography support the diagnosis of brain death, the presence of CBF and glucose metabolism should not alter this conclusion.