Ductus arteriosus dilatation by prostaglandin E1 in infants with pulmonary atresia.
Infants with pulmonary atresia depend on patency of the ductus arteriosus for survival in the immediate postnatal period. Despite continuing hypoxemia after birth the ductus arteriosus usually constricts, thus reducing pulmonary blood flow. This often occurs while awaiting surgical palliation or correction, leading either to marked deterioration in the infant's condition, or death. In ten infants with pulmonary atresia, we infused prostaglandin E1 (PGE1) at a rate of 0.1 mug/kg/min in six and 0.05 mug/kg/min in four into the descending aorta at the orifice of the ductus arteriosus. The ductus arteriosus was effectively dilated; at the narrowest point the diameter, measured in eight infants, almost doubled. In all ten infants arterial blood PO2 increased, averaging 24.6 mm Hg before and 43.7 mm Hg after the infusion was started. Infusion of PGE1 directly into the aorta adjacent to the ductus arteriosus avoided the complications of pyrexia, muscular twitching, and excitability which may be related to the effects of prostaglandins on the central nervous system.[1]References
- Ductus arteriosus dilatation by prostaglandin E1 in infants with pulmonary atresia. Heymann, M.A., Rudolph, A.M. Pediatrics (1977) [Pubmed]
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