Abstract

Periventricular, intraventricular hemorrhage (PIVH) occurs after birth in about 43% of all neonates with birth weights less than 1,500 g. They are believed to be the result of hemodynamic changes in the vascular beds of the germinal matrix or the choroid plexus. Immaturity of the vascular structures and their supporting stroma and inadequacy of hemostatic mechanisms in the premature newborn may contribute to the hemorrhages. Often, PIVH is not isolated and may be an identifiable marker for a brain that has suffered more than one type of lesion. A substantial proportion of affected survivors suffer brain damage. Hypotheses of pathogenesis have been tendered from results of autopsy and from clinical and laboratory studies. It has been proposed that hemorrhages may occur after asphyxial-ischemic episodes, after cerebral arterial or venous hypertension, and/ or during periods of cerebral hyperemia following ischemia. The asphyxiated premature neonates may be more subject to cerebral hypotension

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