Background:The pathophysiology of lethal head trauma in infants and young children involves repetitive rotational forces of sufficient magnitude to produce subdural hemorrhage and brain swelling,which leads to conside...Background:The pathophysiology of lethal head trauma in infants and young children involves repetitive rotational forces of sufficient magnitude to produce subdural hemorrhage and brain swelling,which leads to considerable morbidity and mortality.The precise mechanism for brain swelling is unclear.Materials and Methods:We examined cerebral tissue from ten pediatric deaths due to blunt force trauma,along with seven control infants who asphyxiated in unsafe sleep environments.To assess the competence of the blood-brain barrier,we performed immunohistochemical stains for albumin and immunoglobulin G(IgG).Results:IgG and albumin were increased in subpial and superficial perivascular tissue in those cases due to blunt force trauma,and in particular,the blunt force trauma associated with subdural hematoma.This included two deaths at the scene without hospital survival time.Conclusions:Our findings suggest disruption of the blood-brain barrier with vasogenic edema as an early event in head trauma involving young children upstream of global ischemic brain injury.We hypothesize that mechanical injury to the cortical vasculature results in vasogenic edema by oncotic(increased plasma proteins in the cortical interstitium)and hydrostatic(increased capillary pressure)mechanisms,with subsequent cortical ischemia.This may explain why ischemic sequelae appear to occur in head trauma involving young children,regardless of whether anoxia,hypotension,or cardiac arrest complicate the disease course and may in part underlie the high morbidity and mortality of head trauma in early childhood.展开更多
文摘Background:The pathophysiology of lethal head trauma in infants and young children involves repetitive rotational forces of sufficient magnitude to produce subdural hemorrhage and brain swelling,which leads to considerable morbidity and mortality.The precise mechanism for brain swelling is unclear.Materials and Methods:We examined cerebral tissue from ten pediatric deaths due to blunt force trauma,along with seven control infants who asphyxiated in unsafe sleep environments.To assess the competence of the blood-brain barrier,we performed immunohistochemical stains for albumin and immunoglobulin G(IgG).Results:IgG and albumin were increased in subpial and superficial perivascular tissue in those cases due to blunt force trauma,and in particular,the blunt force trauma associated with subdural hematoma.This included two deaths at the scene without hospital survival time.Conclusions:Our findings suggest disruption of the blood-brain barrier with vasogenic edema as an early event in head trauma involving young children upstream of global ischemic brain injury.We hypothesize that mechanical injury to the cortical vasculature results in vasogenic edema by oncotic(increased plasma proteins in the cortical interstitium)and hydrostatic(increased capillary pressure)mechanisms,with subsequent cortical ischemia.This may explain why ischemic sequelae appear to occur in head trauma involving young children,regardless of whether anoxia,hypotension,or cardiac arrest complicate the disease course and may in part underlie the high morbidity and mortality of head trauma in early childhood.
