TY - JOUR
T1 - Gastric-Outlet Obstruction Induced by Prostaglandin Therapy in Neonates
AU - Peled, Nathan
AU - Dagan, Ovdi
AU - Babyn, Paul
AU - Silver, Meredith M.
AU - Barker, Geoffrey
AU - Hellmann, Jonathan
AU - Scolnik, Dennis
AU - Koren, Gideon
PY - 1992/8/20
Y1 - 1992/8/20
N2 - 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. 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. 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<0.001) or the 4 neonates with clinical signs of gastric obstruction (119±60 hours, P<0.05). The cumulative dose of prostaglandin E1 was higher in the neonates with antral hyperplasia (2982±1392 μg per kilogram of body weight) than in the normal neonates (279±270 μg per kilogram, P<0.001) or the neonates with signs of gastric obstruction (528±306 μg per kilogram, P<0.01). In two neonates with antral hyperplasia, the cessation of therapy lessened the gastric-outlet obstruction. 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. (N Engl J Med 1992;327:505–10.), PROSTAGLANDIN E1 infusion is widely used to maintain patency of the ductus arteriosus in neonates with congenital heart disease, and also to treat persistent fetal circulation and pulmonary hypertension in newborns.1 , 2 An infusion rate of 0.05 μg per kilogram of body weight per minute is associated with a high probability of success in maintaining ductal patency1 and a low risk of serious cardiovascular, central nervous system, and respiratory complications.3 After gastric-outlet obstruction due to antral mucosal thickening had been identified in several neonates receiving prostaglandin E1, we studied the association between the drug and this complication. We…
AB - 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. 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. 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<0.001) or the 4 neonates with clinical signs of gastric obstruction (119±60 hours, P<0.05). The cumulative dose of prostaglandin E1 was higher in the neonates with antral hyperplasia (2982±1392 μg per kilogram of body weight) than in the normal neonates (279±270 μg per kilogram, P<0.001) or the neonates with signs of gastric obstruction (528±306 μg per kilogram, P<0.01). In two neonates with antral hyperplasia, the cessation of therapy lessened the gastric-outlet obstruction. 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. (N Engl J Med 1992;327:505–10.), PROSTAGLANDIN E1 infusion is widely used to maintain patency of the ductus arteriosus in neonates with congenital heart disease, and also to treat persistent fetal circulation and pulmonary hypertension in newborns.1 , 2 An infusion rate of 0.05 μg per kilogram of body weight per minute is associated with a high probability of success in maintaining ductal patency1 and a low risk of serious cardiovascular, central nervous system, and respiratory complications.3 After gastric-outlet obstruction due to antral mucosal thickening had been identified in several neonates receiving prostaglandin E1, we studied the association between the drug and this complication. We…
UR - http://www.scopus.com/inward/record.url?scp=0026773450&partnerID=8YFLogxK
U2 - 10.1056/NEJM199208203270801
DO - 10.1056/NEJM199208203270801
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C2 - 1635565
AN - SCOPUS:0026773450
SN - 0028-4793
VL - 327
SP - 505
EP - 510
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 8
ER -