Ductus Arteriosus Dilatation by Prostaglandin E1 in Infants With Pulmonary Atresia

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Abstract
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 10 infants with pulmonary atresia, prostaglandin E1 (PGE1) was infused at a rate of 0.1 .mu.g/kg/min in 6 and 0.05 .mu.g/kg per min in 4 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 8 infants, almost doubled. In all 10 infants arterial blood PO2 [O2 tension] 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 CNS.