BACKGROUND: An infusion of prostaglandin E1 is widely used to maintain patency of the ductus arteriosus in neonates with congenital heart disease. After gastric-outlet obstruction was recognized in several infants who received prostaglandin E1, we studied the association between the drug and this complication. METHODS: We evaluated all neonates who received prostaglandin E1 in our hospital between October 1, 1989, and September 30, 1991, for clinical, radiologic, or pathological evidence of acute gastric-outlet obstruction. RESULTS: Of the 74 neonates evaluated, 65 had no signs of gastric obstruction and were considered normal; 5 had clinical and radiologic or pathological evidence of gastric obstruction consistent with the presence of antral mucosal hyperplasia. The remaining four neonates had clinical signs of gastric obstruction, but no radiologic or pathological examinations were performed. The 5 neonates with antral hyperplasia had received prostaglandin E1 for longer periods (mean [+/- SD] duration, 569 +/- 341 hours) than the 65 normal neonates (54 +/- 58 hours, P less than 0.001) or the 4 neonates with clinical signs of gastric obstruction (119 +/- 60 hours, P less than 0.05). The cumulative dose of prostaglandin E1 was higher in the neonates with antral hyperplasia (2982 +/- 1392 micrograms per kilogram of body weight) than in the normal neonates (279 +/- 270 micrograms per kilogram, P less than 0.001) or the neonates with signs of gastric obstruction (528 +/- 306 micrograms per kilogram, P less than 0.01). In two neonates with antral hyperplasia, the cessation of therapy lessened the gastric-outlet obstruction. CONCLUSIONS: The administration of prostaglandin E1 to neonates can cause gastric-outlet obstruction due to antral hyperplasia. Neonates who receive prostaglandin E1 at recommended doses for more than 120 hours should be closely monitored for evidence of antral hyperplasia.
BACKGROUND: An infusion of prostaglandin E1 is widely used to maintain patency of the ductus arteriosus in neonates with congenital heart disease. After gastric-outlet obstruction was recognized in several infants who received prostaglandin E1, we studied the association between the drug and this complication. METHODS: We evaluated all neonates who received prostaglandin E1 in our hospital between October 1, 1989, and September 30, 1991, for clinical, radiologic, or pathological evidence of acute gastric-outlet obstruction. RESULTS: Of the 74 neonates evaluated, 65 had no signs of gastric obstruction and were considered normal; 5 had clinical and radiologic or pathological evidence of gastric obstruction consistent with the presence of antral mucosal hyperplasia. The remaining four neonates had clinical signs of gastric obstruction, but no radiologic or pathological examinations were performed. The 5 neonates with antral hyperplasia had received prostaglandin E1 for longer periods (mean [+/- SD] duration, 569 +/- 341 hours) than the 65 normal neonates (54 +/- 58 hours, P less than 0.001) or the 4 neonates with clinical signs of gastric obstruction (119 +/- 60 hours, P less than 0.05). The cumulative dose of prostaglandin E1 was higher in the neonates with antral hyperplasia (2982 +/- 1392 micrograms per kilogram of body weight) than in the normal neonates (279 +/- 270 micrograms per kilogram, P less than 0.001) or the neonates with signs of gastric obstruction (528 +/- 306 micrograms per kilogram, P less than 0.01). In two neonates with antral hyperplasia, the cessation of therapy lessened the gastric-outlet obstruction. CONCLUSIONS: The administration of prostaglandin E1 to neonates can cause gastric-outlet obstruction due to antral hyperplasia. Neonates who receive prostaglandin E1 at recommended doses for more than 120 hours should be closely monitored for evidence of antral hyperplasia.