To test the hypothesis that characteristics of perinatal infection are associated with long‐term cognitive limitations among preterm infants, we analyzed data from 294 infants (142 females, 152 males) ≤1500g birthweight and <37 completed weeks of gestation who were examined at age 9 years. We identified 47 children (20 females, 27 males) who had a non‐verbal Kaufman Assessment Battery for Children (K‐ABC) scale standard value below 70, i.e. more than 2 SDs below the age‐adjusted mean. The 247 children (122 females, 125 males) with a score ≥70 served as control participants. Maternal nationality and education, and low gestational age were significantly associated with a K‐ABC non‐verbal standard value <70. Both neonatal brain damage (intraventricular hemorrhage) and long‐term sequelae (cerebral palsy [CP], diagnosed at age 6 years) were significantly associated with a below‐normal non‐verbal K‐ABC score. Maternal fever at birth was present in five cases (11%) and eight controls (3%; odds ratio 3.6, 95% confidence interval 1.1 to 11.4). Clinical chorioamnionitis and preterm labor and/or premature rupture of membranes (as opposed to toxemia and other initiators of preterm delivery) were also more common among cases than control participants. When adjusting for potential confounders such as gestational age, maternal education and nationality, and CP, the risk estimate for maternal fever remained unchanged (3.8, 0.97 to 14.6). We conclude that perinatal infection might indeed contribute to an increased risk for long‐term cognitive deficits in preterm infants.
To test the hypothesis that characteristics of perinatal infection are associated with long-term cognitive limitations among preterm infants, we analyzed data from 294 infants (142 females, 152 males) < or = 1500 g birthweight and <37 completed weeks of gestation who were examined at age 9 years. We identified 47 children (20 females, 27 males) who had a non-verbal Kaufman Assessment Battery for Children (K-ABC) scale standard value below 70, i.e. more than 2 SDs below the age-adjusted mean. The 247 children (122 females, 125 males) with a score > or = 70 served as control participants. Maternal nationality and education, and low gestational age were significantly associated with a K-ABC non-verbal standard value <70. Both neonatal brain damage (intraventricular hemorrhage) and long-term sequelae (cerebral palsy [CP], diagnosed at age 6 years) were significantly associated with a below-normal non-verbal K-ABC score. Maternal fever at birth was present in five cases (11%) and eight controls (3%; odds ratio 3.6, 95% confidence interval 1.1 to 11.4). Clinical chorioamnionitis and preterm labor and/or premature rupture of membranes (as opposed to toxemia and other initiators of preterm delivery) were also more common among cases than control participants. When adjusting for potential confounders such as gestational age, maternal education and nationality, and CP, the risk estimate for maternal fever remained unchanged (3.8, 0.97 to 14.6). We conclude that perinatal infection might indeed contribute to an increased risk for long-term cognitive deficits in preterm infants.
371 long-term surviving very low-birth-weight (VLBW) infants born between July 1983 and June 1986 with a birthweight under 1501 g were followed-up. This sample amounted to 91% of such infants of six neonatal intensive care units in Hamburg (Germany). A neurological examination and a developmental evaluation using the Griffith Developmental Scale were carried out at the age of 18 to 20 months, corrected for gestational age. Ninety-six of the 371 infants were small for gestational age (SGA), 275 appropriate for gestational age (AGA). Striking differences between these two groups were found concerning perinatal risk factors and neurological outcome. Maternal risk factors associated with intrauterine growth retardation such as maternal toxemia and signs of fetal stress were found in a high percentage of the mothers of SGA-children, factors associated with premature labor and chorioamnionitis in mothers of AGA-children. Cerebral palsy was detected in only 7% of the SGA-children but 17.5% of the AGA-children. The difference in the development of cerebral palsy was attributed mainly to different postconceptual ages of the SGA- and AGA-children. In general, minor neurological abnormalities were detected in as many as 30% of SGA- and only 15.3% of AGA-children. None of the SGA-children over 33 weeks of gestational age developed cerebral palsy, but 25% minor neurological abnormalities. As to cerebral palsy the prognosis of SGA-infants with a very low birthweight is not different from AGA-infants with a similar gestational age. Regarding the development of minor neurological abnormalities, however, intrauterine growth retardation seems to be a risk factor independent from gestational age.
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