840
E d i t o r i a l correspondence
REFERENCES
1. Cowan F. Indomethacin, patent ductus arteriosus and cerebral blood flow J PEDIATR 1986;109:341-3. 2. Simeoni U, Messer J, Weisburd P, Haddad J, Willard D. Neonatal renal dysfunction and intrauterine exposure to prostaglandin synthesis inhibitors. Eur J Pediatr 1989;148:371-3.
Reply To the Editor: We find the experience of Haddad et al. to be interesting. However, the circumstance under which they administered indomethacin was different. They gave indomethacin prenatally, and thus any effect on the fetus should take into account both associated anatomic and circulatory changes. In utero closure of the patent ductus arteriosus may occur with indomethacin administration, resulting in a major fetal circulatory disturbance. Cerebral ischemia is not unlikely. Furthermore, the abnormality that led to premature labor, and thus the necessity for prenatal administration of indomethacin, may have been a major contributing factor in the development of cerebral ischemia and periventricular leukomalacia. A decreased urinary concentration of prostaglandin E2 merely suggests an indomethacin effect (primarily renal). A causal relationship between prenatal indomethacin administration and fetal cerebral ischemic injury is speculative at best. As to the influence of antenatal factors on neonatal cerebral abnormality, we prospectively evaluated 230 mothers whose fetuses had an estimated weight of _< 1750 gm and who were anticipating premature delivery because of premature labor or other reasons. One hundred thirty-two did not receive tocolytic agents, and 92 received tocolytic agents other than indomethacin. Six other mothers had antenatal indomethacin but only after failure of response to other tocolytic agents. To minimize the influence of neonatal intensive care factors on the development of neonatal cranial ultrasound abnormalities, the first scan was performed within minutes of delivery (--
E d i t o r i a l correspondence
REFERENCES
1. Cowan F. Indomethacin, patent ductus arteriosus and cerebral blood flow J PEDIATR 1986;109:341-3. 2. Simeoni U, Messer J, Weisburd P, Haddad J, Willard D. Neonatal renal dysfunction and intrauterine exposure to prostaglandin synthesis inhibitors. Eur J Pediatr 1989;148:371-3.
Reply To the Editor: We find the experience of Haddad et al. to be interesting. However, the circumstance under which they administered indomethacin was different. They gave indomethacin prenatally, and thus any effect on the fetus should take into account both associated anatomic and circulatory changes. In utero closure of the patent ductus arteriosus may occur with indomethacin administration, resulting in a major fetal circulatory disturbance. Cerebral ischemia is not unlikely. Furthermore, the abnormality that led to premature labor, and thus the necessity for prenatal administration of indomethacin, may have been a major contributing factor in the development of cerebral ischemia and periventricular leukomalacia. A decreased urinary concentration of prostaglandin E2 merely suggests an indomethacin effect (primarily renal). A causal relationship between prenatal indomethacin administration and fetal cerebral ischemic injury is speculative at best. As to the influence of antenatal factors on neonatal cerebral abnormality, we prospectively evaluated 230 mothers whose fetuses had an estimated weight of _< 1750 gm and who were anticipating premature delivery because of premature labor or other reasons. One hundred thirty-two did not receive tocolytic agents, and 92 received tocolytic agents other than indomethacin. Six other mothers had antenatal indomethacin but only after failure of response to other tocolytic agents. To minimize the influence of neonatal intensive care factors on the development of neonatal cranial ultrasound abnormalities, the first scan was performed within minutes of delivery (--
