Persisting Ductus Arteriosus and Intraventricular Hemorrhage

Abstract

8Particular morphological and functional conditions of the immature brain predispose preterm infants to intraventricular hemorrhage (IVH). Cerebral PerfusionAs a source of neuronal and glial precursors the subependymal germinal matrix is a proliferative tissue, which is richly vascularized. Cerebral autoregulation, which provides constant cerebral blood flow over a broad range of arterial blood pressure in adults, is not as effective in preterm infants (⊡ Fig. 8.1). Therefore, alterations in arterial blood pressure provoke fluctuations in the cerebral blood flow of preterm infants, which may lead to rupture of the vulnerable capillaries of the subependymal germinal matrix resulting in IVH.Patent ductus arteriosus (PDA) is well known to influence the arterial blood pressure and to alter cerebral blood flow. Thus, the question arises whether PDA is capable of causing IVH in preterm infants. This assumption is highly suggestive because PDA and IVH occur within the same population. Incidence of both PDA and IVH increases with decreasing birth weight and decreasing gestational age [8,9]. However, about 50% of all IVH occur during the first day of life, a period before PDA usually becomes clinically symptomatic (⊡ Fig. 8.2). Osborn et al.[11] determined distinct and different risk factors for early and late periventricular/intraventricular hemorrhage in two large prospective cohort studies with a total of 254 infants born before 30 weeks gestation. Low superior vena cava flow (SVC) in the first 24 hours of life was the only independent risk factor associated with IVH in both cohorts. Adjusted for the perinatal risk factors, low SVC flow was associated with a large ductus diameter in the first cohort [12]. PDA, Lung Maturity, and IVHBoth PDA and IVH are associated with respiratory distress syndrome (RDS) in preterm infants. Prenatal corticosteroid therapy in order to prevent RDS has been shown to reduce the incidence of both PDA and IVH in preterm infants of 26-34 weeks gestation [1]. Natural surfactant given prophylactically to preterm infants of less than 30 weeks gestation effectively reduces neonatal mortality and the incidence of pulmonary air leaks, but does not significantly reduce the rate of PDA and IVH [10]. Thus, prevention of RDS by prenatal steroids but not by surfactant is combined with lower incidence of both