Persistent pulmonary hypertension of the newborn (PPHN) is a life
threatening condition associated with an increased risk of
neurodevelopmental impairment. The recommended treatment for this
condition is inhaled nitric oxide (iNO) and has been used in our
Neonatal Intensive Care Unit since 1998. We prospectively offered
neurodevelopmental follow-up to children treated with iNO for PPHN,
including extensive neurological evaluation, developmental/cognitive
evaluation at 18 months and 3.5-5 years old, and evaluated the rate of
severe and moderate handicap and normal neurodevelopmental
outcome, compared to a control group and the literature. Population
consisted of 29 patients treated only with iNO, born between 01.01.1999
and 31.12.2005 (study group), and 32 healthy term infants born in 1998
in our maternity (control group). During those seven years, 65 infants
were admitted in our Unit with PPHN, of whom 40 were treated with iNO
alone. 34 children survived (85%) and were offered neurodevelopmental
follow-up, 7 children were lost to follow-up due to various reasons. 22
children were examined at the age of 18 months (76%) with a rate of
moderate handicap of 22% (2 with expressive language delay, 2 with
difficult behavior, and 1 child with moderate hearing loss), and a rate of
major handicap of 4.5% (1 child with cerebral palsy due to perinatal
stroke, and moderate hearing loss). At preschool age, 17 (50%) were
examined, the rate of moderate handicap was 22% (4 borderline
intelligence, 1 hearing loss), and the rate of major handicap was 4.5%
(one child with cerebral palsy and hearing loss), compared to 26.9%
and 0% in the control group. Mean developmental quotient at 18 months
was 100.3 ± 8.7 (control group 118.3), and at preschool age mean
cognitive indices were within normal limits for the 2 tests performed at
3.5 or 5 years (108 ± 21, 94.4 ± 17). Most of the children with a less
favorable neurodevelopmental outcome suffered from birth asphyxia
(ruptured uterus, placental abruption, maternal hypotension, diabetic
cardiomyopathy), and notably, the 2 children with sensorineural hearing
loss both suffered from severe hypoxic-ischemic enkelopathy. Treatment
with iNO was not the direct cause of the neurodevelopmental
impairments observed in children treated for PPHN.