The prognosis of perinatal brain damage was studied prospectively in a one year birth cohort of 12,000 children born in Northern Finland in 1966. Children were included in the study if they had an Apgar score of 0 at 1 min or less than 5 at 15 min, convulsions during the neonatal period, or a diagnosis of asphyxia, brain injury or intraventricular haemorrhage, but did not have CNS malformation, chromosomal aberrations or hereditary CNS degeneration. There were 233 children, 19.3 per thousand, of which 134, 58.0% were boys. Eighty-four, 36.4% died during the first 28 days and 7 children died before the age of 14 years, 6 of the latter group being handicapped. There were 44 children, 29.9% who had mental retardation, IQ less than 71, epilepsy or cerebral palsy. With regard to these children 13 had normal school performance, but there were 12 other children in the perinatal brain damage group who needed special education, two of them because of deafness. Perinatal brain damage accounted for 57.5% of all neonatal deaths, 30% of admissions to a special nursery and 12.5% of mental retardation (IQ less than 71), epilepsy and cerebral palsy at the age of 14.
The activities of two gluconeogenic enzymes, glucose-6-phosphatase and fructose-1,6-diphosphatase were examined in the normal and intrauterine growth retarded (IUGR) rat during the first 5 days of life. The fructose-1,6-diphosphatase activity, 1.54 +/- 0.10 mumol/min/g liver (means +/- SEM) in control and 1.47 +/- 0.20 in the IUGR rats, increased in both groups on days 2--4 but remained significantly lower in the IUGR rats through day 4 (4.53 +/- 0.6 mumol/min/g liver in control and 3.09 +/- 0.22 mumul/min/g liver in the IUGR rats, P less than 0.01). The glucose-6-phosphatase activity increased similarly in both groups. The weight of the IUGR rats remained lower through the third postnatal day (6.47 +/- 0.42 compared to 8.64 +/- 0.27 g in control rats). Blood glucose concentrations at birth were 117 +/- 11 mg/dl in control rats and 73 +/- 11 mg/dl in the IUGR rats (P less than 0.01). Although the glucose concentrations increased in both groups on days 2--4, the IUGR rats maintained relatively lower levels (P less than 0.01). The results indicate that IUGR fetal rats do not have augmented gluconeogenesis in spite of hypoglycemia. In addition, effective gluconeogenesis in the neonatal period appears to be delayed.
Proportional assist ventilation (PAV) amplifies the ventilatory effect of the spontaneous respiratory effort and therefore allows analysis of drug-induced changes in the spontaneous breathing pattern of subjects who depend on mechanical ventilatory assistance. We hypothesized that theophylline will reduce the number and duration of respiratory pauses and apneic events in infants less than 1000 g of birth weight on PAV. Twelve infants were studied: median birth weight was 773 g; gestational age 26.0 weeks and postnatal age 9 days. Measurements were obtained over a 2-h period before and after 5 mg/kg of intravenous theophylline. A respiratory pause was defined as cessation of breathing for at least the duration of three preceeding breaths. The total number of respiratory pauses and the number of apneas followed by either cardiac slowing (decrease in heart rate more than 10%) or bradycardia decreased significantly. Minute ventilation increased due to a rise in tidal volume from 5.6+/-1.3 to 6.1+/-1.2 ml/kg (p=0.004). The duration of respiratory pauses, the respiratory rate, and the number of apneas followed by desaturation did not change significantly. We conclude that theophylline stimulates spontaneous breathing in infants less than 1000 g, reduces the number of apneas, and increases minute volume by increasing the tidal volumes.
We studied the nutritional requirements of 53 neonates with a birth-weight of 1250 g or less and analysed the parenteral and enteral nutrition provided, the weight-gain curves, the incidence of prior pathology and complications. We compared those weighing under 1000 g at birth (n=25) with those weighing 1001-1250 g (n=28). All neonates received central parenteral nutrition at an average age of 42.3 h. The liquid requirements of the lower birth-weight group were significantly greater. No differences were found in the supply of glucose, proteins, lipids and calories until after the first 15 days of life, when the <1000 g group required a greater liquid and caloric intake. Parenteral nutrition was suspended earlier for the >1000 g group (32.6 vs. 48.1 days). Maximum weight loss (12.56%) for the two groups occurred at 5.23 days. No differences in weight gain (g/kg/day) between the groups were observed. The >1000 g group began enteral nutrition significantly earlier and presented greater tolerance. The incidence of complications (bronchopulmonary dysplasia, enterocolitis, nosocomial sepsis, Candidas A sepsis, osteopenia) was greater in the lower birth-weight group, as was that of hyaline membrane disease and mechanically assisted respiration. There were no differences in the incidence of intracraneal haemorrhage, ductus arteriosus, early sepsis, delayed intrauterine growth or hypoglucemia.
The severity of the initial pathology and the greater incidence of complications among the lower birth-weight neonates (<1000 g) influenced both the need for parenteral nutrition and the reduced tolerance to enteral nutrition. Although the rate of weight gain was similar for the two groups, the <1000 g group required a longer period of parenteral nutrition.
We measured extracellular fluid volume by bromide dilution within 12 h of birth in 32 infants less than 1000 g birth weight. Mean (+/- S.D.) birth weight and gestational age were 763 +/- 123 g and 26 +/- 1 week, respectively. Mean extracellular fluid volume was 360 +/- 86 ml (477 +/- 107 ml/kg). These results are similar to extracellular fluid volume estimates from previous carcass analysis data. Wide variability is observed with both methods suggesting that biologic variability may be important.
The major objective of this study was to determine whether the embryo biopsy procedure might cause growth restriction or affect health outcome of children.
Auxological data and physical findings were compared at birth and age 2 for 102 children (70 singletons and 32 twins) born after PGD/PGS and 102 matched children born after intracytoplasmic sperm injection (ICSI) in a prospective study.
No statistically significant differences regarding weight, height and head circumference standard deviation scores (SDS) at birth and at age two years were observed. At two years of age the mean BMI SDS tended to be lower in PGD/PGS children (p=0.058). PGD/PGS babies had been more often breastfed (p=0.013), but mostly during a shorter time. The prevalence of major as well as minor congenital anomalies, hospital admissions and surgical interventions was similar.
Children born after embryo biopsy applied in PGD/PGS present similar prenatal and postnatal growth and health outcome in the first two years of life compared to ICSI children. Up till now, PGD and PGS appear not to be associated with a higher risk for health problems.
To clarify whether openning of the uterine isthmus between 11 and 13weeks' gestation adversely affects the placental development.
The uterine cervix and isthmus lengths were measured prospectively using transabdominal ultrasound at 11 to 13+6weeks' gestation. Following delivery, the pregnancy and delivery course were reviewed. The associations between the conditions of the uterine isthmus during the first trimester and the perinatal complications associated with placental abnormalities were analyzed.
A total of 653 cases were analyzed. The isthmus had been completely opened (isthmus length=0mm) in 15.9%, 21.6% and 24.1% of the cases at 11, 12 and 13weeks' gestation. The frequencies of perinatal complications in the cases whose isthmus had been opened (cases) and the other cases (controls) were as follows; 1.4% and 1.0% (ns) for placenta previa, 1.4% and 1.2% (ns) for abnormal cord insertion, 3.5% and 4.3% (ns) for pre-eclampsia, 9.9% and 9.0% (ns) for small for gestational age, and 12.0% and 7.6% (ns) for preterm delivery, respectively.
Early opening of the uterine isthmus at 11 to 13weeks' gestation does not appear to adversely affect either the placental development or the course of pregnancy.
De novo lipid synthesis can be demonstrated in human fetal subcutaneous tissue cells which are in the initial stages of liquid accumulation. Lipogenic capacity measured as ability to incorporate acetate into neutral lipid was shown to increase with gestational age. This lipogenic capacity was accompanied by an increased activity of acetyl co-enzyme A carboxylase. Insulin, which is known to activate this enzyme in mature adipose tissue, increased neutral lipid synthesis in fetal subcutaneous tissue. When tissue insulin levels were determined, insulin was found from 16 wk gestation. At this time triglyceride content of the tissue was also increasing. Thus de novo fatty acid synthesis is a means by which the developing adipose cell initiates lipid accumulation.
Chimaeric fusion genes derived by chromosome translocation are common molecular abnormalities in paediatric leukaemia and provide unique markers for the malignant clone. They have been especially informative in studies with twins concordant for leukaemia and in retrospective scrutiny of archived neonatal blood spots. These data have indicated that, in paediatric leukaemia, the majority of chromosome translocations arise in utero during foetal haemopoiesis. Chromosomal translocations and preleukaemic clones arise at a substantially higher frequency ( approximately 100x) before birth than the cumulative incidence or risk of disease, reflecting the requirement for complementary and secondary genetic events that occur postnatally. A consequence of the latter is a very variable and occasionally protracted postnatal latency of disease (1-15 years). These natural histories provide an important framework for consideration of key aetiological events in paediatric leukaemia.
The brains of 50 consecutively admitted infants weighing 1250 g or less at birth were serially examined beyond the neonatal period for periventricular haemorrhage and for periventricular leukomalacia with real-time ultrasound. There was significant correlation between the presence or absence and the severity of haemorrhage with survival. A prospective neurodevelopmental assessment was completed at 2 years of age, corrected for prematurity, on all survivors. None of the 20 survivors with normal scans or germinal layer haemorrhages had evidence of major disability and all four survivors with intracerebral haemorrhage or periventricular leukomalacia had major disability. The mental performance on the Bayley scales of infant development was also significantly worse in the latter group. Six of the eight survivors with intraventricular haemorrhage had no major disability, including three who had post-haemorrhagic hydrocephalus. Our results showed that cerebral ultrasound detection of brain pathology is a good predictor of neurodevelopmental outcome in such extremely low birthweight infants. However, as the maximum extent of periventricular haemorrhage may develop beyond one week of age and cystic periventricular leukomalacia commonly develops after the neonatal period, serial scanning is mandatory to ensure diagnostic accuracy for both periventricular haemorrhage and leukomalacia.
Near-infrared spectroscopy is a non-invasive method of assessing cerebral oxygenation. Functional echocardiography is increasingly used by neonatologists in the assessment of cardiovascular function.
To correlate cerebral tissue oxygenation index (cTOI) and cardiac output in infants less than 1250 g at 6, 12, 24 and 48 hours of age.
A prospective observational study.
Newborns with birth weight<1250 g.
Serial assessments of superior vena cava (SVC) flow, right and left ventricular outputs, ductus arteriosus and cTOI were performed at 6, 12, 24 and 48 hours of age. Clinical parameters, including mean blood pressure, mean airway pressure, blood gas parameters and oxygen saturations were recorded.
22 neonates were enrolled following parental consent. The mean birth weight was 851 g (SD±201), mean gestational age was 25.9 weeks (SD±1.7). Mean SVC flow at 6 hours of age was 56.8 ml/kg/min and increased to 68.6 ml/kg/min at 48 hours of age. 9 infants (41%) had at least one measurement of low SVC flow (<41 ml/kg/min) in the first 48 hours. Mean cTOI was 65.2% at 6 hours of age, 63.9% at 12 hours of age, 68.8% at 24 hours of age and 67.2% at 48 hours of age. Cerebral fractional tissue oxygen extraction values were highest at 12 hours (0.31±0.09). There was no correlation between SVC flow and cTOI values.
SVC flow, left and right ventricular output increased during first 48 hours of life. cTOI decreased at 12 hours of age with a concomitant increase in fractionated oxygen extraction. These changes reflect transitional changes in both cardiac and cerebral hemodynamics in extremely low gestational age newborns during the first 48 hours.
In determining the detectability of brainstem, middle latency and cortical auditory evoked responses in preterm newborns, one has to deal with the ongoing maturation of the auditory system. In the preterm period the detectability of evoked responses is closely related to the appearance of the individual evoked response components. The detectability of the individual evoked response components in preterm infants is important, because low detectability rates make the absence of a particular evoked response component irrelevant with respect to the clinical-neurophysiological correlation. In a longitudinal study we determined the detectability and cumulative detectability, i.e. the presence of individual evoked response components in one or more recordings of evoked response components in 37 low risk preterm infants between 30 and 41 weeks conceptional age (CA). On the basis of their detectability it is concluded that evoked response components, determined between 30 and 34 weeks CA, are generally of limited use for clinical application, except for auditory brainstem response (ABR) components I, IIn, V and Vc and middle latency response (MLR) component Na. Our study made clear that improvement can be achieved by performing more than one examination within a period of approximately 4 weeks between the recording sessions. The cumulative detectability rates after two recordings showed improvement for all components involved in this study. The cumulative detectability rates of ABR components I, II, IIN, III, V, IIc, IIINc, Vc, MLR components Na and P0, and auditory cortical response (ACR) components PbP1 and N2p are sufficient to use as measures in the neurophysiological judgement of functional integrity of the central auditory pathway in preterm infants.
Pre-term infants are at high risk for motor disabilities. Postural control, the basis for motor development, develops rapidly during the first year of life. An early start to extra-uterine life with an immature motor system may influence a pre-term infant's postural control.
To identify important prognostic factors and determine the difference in postural control between full-term and pre-term infants.
Medical records of 93 pre-term infants with birth weight of less than 1501g (mean birth weight=1136.03+/-243.86g; mean gestational age=29.14+/-2.78 weeks) were reviewed. Data was collected from the preemie clinical follow-up program at the National Cheng Kung University, Taiwan.
Results demonstrated that pre-term infants had poorer postural control than full-term infants both at 6 and 12 months adjusted age, and that medical complication as measured by the Neonatal Medical Index was the best predictor of postural control in pre-term infants in the first year of life. In addition, our findings confirmed that the development of postural control at 6 months adjusted age predicts the development of postural control at 12 months adjusted age after controlling for prognostic factors.
Both biological and social environmental factors appeared to be associated with pre-term infants' postural control at 6 and 12 months adjusted age. The development of postural control at 6 months adjusted age predicted the development of postural control at 12 months adjusted age. This suggested the value of early follow-up examinations at 6 months adjusted age.
Maternal serum SP1 concentration was measured at 10-13 weeks' gestation in samples from 87 pregnancies with fetal chromosomal abnormalities (trisomy 21 n = 45; trisomy 18 n = 19; trisomy 13 n = 8; Turner syndrome n = 7; 47,XXX or 47,XXY n = 4; triploidy n = 4), and in samples from 348 matched controls. In the control group, SP1 increased significantly with fetal crown-rump length (r = 0.20, P < 0.0001) and there was no significant association with fetal nuchal translucency thickness (r = 0.03). Similarly, in the group with fetal chromosomal abnormalities, SP1 increased significantly with crown-rump length (r = 0.31, P < 0.01) and there was no significant association with nuchal translucency thickness (r = -0.08). In the groups with fetal trisomy 18 and trisomy 13, the median SP1 (0.76 MoM and 0.57 MoM, respectively) was significantly lower than in the controls (z = 2.64 and z = 3.27, respectively); in 21% and 25% of the cases, values were below the 5th centile. In the group with trisomy 21 and other chromosomal abnormalities the median SP1 (0.96 MoM and 0.93 MoM, respectively) was not significantly different from controls (z = 1.17 and z = 0.67, respectively). Measurement of SP1 concentration at 10-13 weeks' gestation is not likely to be useful in the prediction of fetal chromosomal abnormalities.
Few studies have evaluated the reasons why lethal chromosomal anomalies continue to occur despite the importance of this question for maximizing perinatal care.
To determine why trisomy 13 or 18 births continue to occur in Alaska.
Case series involving review of maternal and infant medical records.
All 28 known infants and fetuses that died with trisomy 13 or 18 during 1992-2001 and their mothers.
The proportion of mothers that declined or received a variety of routine prenatal tests, the results of prenatal testing, and the impact of testing on decisions related to pregnancy.
Seventeen women declined pregnancy termination or amniocentesis, 10 had no prenatal risk factors and were not offered these procedures, and one woman had an amniocentesis but was not offered pregnancy termination. Twenty-six women had >/=1 prenatal ultrasounds; for 17 women, these were interpreted as normal throughout pregnancy (n=11) or until after 30 weeks gestation (n=6) despite substantial fetal malformations. Fourteen of 15 women with an abnormal ultrasound had an amniocentesis compared to one of eight women whose only risk factor was advanced maternal age.
Most trisomy 13 or 18 deliveries occurred to women who declined amniocentesis or pregnancy termination. Failure to identify abnormalities on prenatal ultrasound may have contributed to the decision not to have these procedures.
Although both very preterm (VP) and small for gestational age (SGA) births are suggested to increase the likelihood of childhood emotional problems, there has been a lack of research comparing these effects.
To investigate levels of emotional problems between 6-13 years of age and contrast the impact of being born either very premature (irrespective of birth weight) or small for gestational age.
Prospective longitudinal cohort study.
654 Bavarian children (born 1985-1986) who were followed from birth to age 12/13 years.
Emotional problems at ages 6.3 and 8.5 years were measured via the Child Behavior Check List (CBCL). Emotional problems were measured at age 12/13 years via the Strengths and Difficulties Questionnaire (SDQ). Trajectories of emotional problems were derived between 6.3 and 13 years.
Two distinctive patterns of age 6-13 year emotional problems were found: 1) a low and stable level of problems in 76% of children; 2) a high and stable level of problems in 24% of children. The high and stable pattern of emotional problems was significantly associated with a VP but not an SGA birth. Consistent additional determinants included male child gender and lower family socioeconomic status.
The disparity between VP and SGA births as a predictor of age 6-13 year old emotional problems is considered in terms of fetal and/or glucocorticoid programming. The stability of emotional problems between 6 and 13 years reinforces the need for early childhood interventions aimed at children born very preterm.
It continues to be a challenge for clinicians to identify preterm infants likely to experience subsequent neurodevelopmental deficits. The Test of Infant Motor Performance (TIMP) and the assessment of spontaneous general movements (GMs) are the only reliable diagnostic and predictive tools for the functionality of the developing nervous system, if applied before term.
To determine to what extent singular preterm assessments of motor performance can predict the neurodevelopmental outcome in 14-month olds.
Thirty-seven preterm infants born <34weeks gestational age were recruited for the study at the NICU of the São Lucas University Hospital, Porto Alegre, RS, Brazil. At 34weeks, their GMs were assessed; and the Test of Infant Motor Performance (TIMP) was applied. A prospective design was used to examine (A) the association between the GM assessment and the TIMP; and (B) the relation between GMs or the TIMP and the developmental status at 14months, assessed by means of Alberta Infant Motor Scales (AIMS) and the Pediatric Evaluation of Disability Inventory (PEDI).
Nineteen infants (41%) had abnormal GMs; only one scored within the TIMP average range. Hence, GMs and TIMP were not related. Children with cramped-synchronized GMs at 34weeks preterm had a lower AIMS centile rank than those with poor repertoire or normal GMs. There was a marginal association between cramped-synchronized GMs and a lower PEDI mobility score.
A single preterm GM assessment is only fairly to moderately associated with the 14-month motor development. The TIMP is not suitable as a complementary assessment tool at such a young age.
Neurodevelopmental and behavioural problems have been repeatedly reported in very preterm survivors, often showing themselves later in childhood as poor school performance. Early identification of problems would mean that appropriate remedial therapy can be implemented. We have previously shown that neurodevelopmental status at 1 year was predictive of outcome at 8 years in a cohort of preterm infants. The aim of this paper was to see if neurodevelopmental outcome in adolescence could be predicted by assessment by 1 year in the same cohort of preterm infants.
Prospective cohort study.
150 adolescents, born before 33 weeks gestation.
Neurological examination, developmental quotient, vision and hearing by 1 year. At 14-15 years, neurological examination, school performance questionnaire, Schonnell test of reading age, a premorbid adjustment score, Rutter behavioural score and for those born from 1981, cognitive tests (WISC-R).
A highly significant relationship existed between neurological status by 1 year and the need for extra educational provision, overall neurodevelopmental status, cognitive function in those that had their IQs measured and premorbid adjustment score of prepsychotic symptoms in adolescence. However, status at 1 year was not predictive of adolescent reading age or behavioural score.
Neurodevelopmental assessment at 1 year is predictive of school performance and outcome in the adolescent period.
A range of adverse birth outcomes is associated with heavy prenatal alcohol exposure.
To examine the effects of moderate levels of alcohol consumption during pregnancy on children's intellectual ability, learning and attention at 14 years of age.
The Mater-University of Queensland Study of Pregnancy involves a prospective birth cohort of 7223 singletons whose mothers were enrolled at the first antenatal visit. At 14 years, 5139 mothers and adolescents completed attentional and learning questionnaires, and 3731 adolescents completed psychometric assessments.
For adolescents, the Wide Range Achievement Test--Revised (WRAT-R) and Raven's Standard Progressive Matrices Test (Raven's) were administered. Mothers completed the Child Behaviour Checklist (CBCL) and adolescents completed the Youth Self Report (YSR). Learning was assessed by a series of questions in the mother and adolescent questionnaires. Maternal measures included the quantity and frequency of alcohol consumption, and the extent of binge drinking.
For consumption of <1 glass/day in early or late pregnancy, there was no association with any attention, learning or cognitive outcomes. The strongest estimates of effect were found among those consuming > or =1 glasses/day. Exposure in late pregnancy was associated with increased prevalence of overall learning difficulty in the unadjusted, although not the adjusted analysis. Binge drinking was associated with a higher prevalence of Raven's score <85 (1 standard deviation).
Although a number of study limitations need to be considered, the results suggest that consumption at the level of <1 drink/day does not lead to adverse outcomes in relation to attention, learning and cognitive abilities, as measured in the current research.
One component of the major transformation of neural functions at the end of the second postnatal month is concerned with a change in the appearance of general movements. These endogenously generated complex movements lose their writhing character and are replaced by a transient form, termed 'fidgety' movements. There are individual differences in the age of onset and duration as revealed by longitudinal observations. It is speculated that 'fidgety' movements may be related to a postnatal calibration of the proprioceptive system.
Studies of the effects of maternal smoking during pregnancy have reported inconsistent findings in relation to measures of offspring cognitive functioning. Few studies, however, have examined learning outcomes in adolescents, as opposed to IQ.
To examine the association between maternal smoking during pregnancy and academic performance among adolescent offspring.
Population-based birth cohort study.
7223 mothers and children were enrolled in the Mater-University of Queensland Study of Pregnancy in Brisbane (Australia) from 1981 to 1984. Analyses were restricted to the 4294 mothers and children for whom all information was reported at 14-year follow-up.
Reports of academic performance of 14-year-old offspring in English, Science and Mathematics with different patterns of maternal smoking (never smoked, smoked before and/or after pregnancy but not during pregnancy, or smoked during pregnancy).
Low academic achievement was more common only in those whose mothers had smoked during pregnancy. Effect sizes were, however, small. The adjusted mean difference in total learning score for smoking before and/or after pregnancy but not during pregnancy, and for smoking during pregnancy were -0.18 (-0.58, 0.22) and -0.40 (-0.69, -0.12). Similarly, the adjusted odds ratios were 0.9 (0. 65, 1.24) and 1.35 (1.07, 1.70).
Maternal smoking during pregnancy is a preventable prenatal risk factor associated with small decrements in offspring academic performance that continue into adolescence.
A fiberscope supported by a holder, devised by one of the authors, was used to film neonatal sucking behaviour and its development from birth to 14 months of life. The subjects were 57 low-risk full term infants. Present observations detect a developmental course of the sucking behaviour. The main changes are: (a) the bell shape produced by the peristaltic tongue movements is quite high in the neonatal period, decreases in height considerably during the third month and almost disappears by the tenth month of life. (b) The depth of the cavity produced by the peristaltic tongue movements increases from the third month until the eighth month and decreases after this time, (c) The wrapping by the root of the tongue at the tip of the nipple gradually weakens during the first month and almost disappears around the sixth month of life. (d) The neonatal pattern disappears and the pattern for older infants appears in one sucking episode in the same infant during the second and third month after birth. There are individual differences in the period of actual change but it usually appears during the third month.
Concentrations of placental protein 14 (PP14) were measured by radioimmunoassay in 103 amniotic fluid samples from 10 to 20 weeks of pregnancy. Low levels of PP14 were present at 10-12 weeks (median values 82-280 micrograms/l). After 12 weeks, the levels increased by two orders of magnitude to reach a peak at 18 weeks (median 11 mg/l). This pattern may reflect the obliteration of the extraembryonic coelom and direct apposition of the decidua with the chorio-amnion.
Little research has examined the associations between early sleep problems and attention problems over several developmental periods.
To examine whether sleep problems in infancy and early childhood are independently related to attention difficulty at 5 and 14 years, and to the continuity of attention difficulties from 5 to 14 years.
The study was a prospective, population-based birth cohort study.
7223 women who delivered a live, singleton child between 1981 and 1983 were recruited at the first antenatal visit. Of these, 4204 had complete information on all key measures.
Attention problems were assessed with items from the Child Behaviour Checklist (CBCL) and were classified as adolescent onset (i.e. problems at 14 but not at 5); early remitter (problems at 5, no problem at 14); and persistent (i.e. at both 5 and 14).
At 6 months, sleep problems 'sometimes' were associated with the early remitter group in boys. For sleep problems between 2 and 4 years of age, findings were generally similar for boys and girls with strong associations with adolescent attention. Sleep problems 'often' were independently associated with early remitter and persistent attention problems, and 'sometimes' with early remitter and adolescent onset attention problems.
Sleep problems in early childhood are an indicator of subsequent attention problems that may persist into adolescence. Whether these associations are causal requires further research, however their presence provides an opportunity for early intervention and monitoring.
Binocular grating acuity was tested in 138 low birth weight (LBW) neonates (birth weights ranging from 1500 to 2500 g) by means of the prototype version of the Acuity Card Procedure. No surrounding screen was used. Mean visual acuity of 107 neonates successfully assessed at mean corrected ages of -1.9 weeks (+/- 1.9 weeks) amounted to 0.58 cycles/degree (S.D. 0.71 octaves). Success rate was 77.5%. Mean postnatal age was 2.3 weeks (+/- 1.6 weeks). Acuity values of various subgroups ranged between 0.68 cycles/degree (S.D. 1.3 octaves) in low-risk, small for gestational age (SGA) preterms (n = 7), to 0.56 cycles/degree (S.D. 0.7 octaves) in SGA fullterms (n = 34), independent whether at low-or at high-risk. These differences were not significant, although with multiple regression analysis with adjustment for corrected age of testing, mean acuity of low-risk preterms was slightly better than of low-risk fullterms (P = 0.055). No significant change of acuity over corrected age could be demonstrated, except for a slight progress (r = 0.57; P less than 0.05) in the subgroup of 13 low-risk fullterms. The high variability of acuity values in neonates and the slow acuity development at term age hamper assessment of differences between various subgroups of neonates.
Growth of very low birthweight (VLBW) infants is used to monitor nutrition and intrauterine velocity is taken as the desired goal.
We hypothesised that beside nutrition growth failure is caused by disease severity.
Prospective longitudinal study of 45 VLBW infants undergoing intensive care, mechanical ventilation was used as proxy to disease severity. Nutritional intake, body weight, length, head circumference, and lower leg length (LLL) were measured during the first 5 weeks of life.
Birthweight and gestational age were lower in 22 ventilated than in 23 unventilated infants (p<0.01). Median daily intake was 3.2 and 2.8 g/kg for protein (n.s.), 108 and 112 kcal/kg for energy (n.s.), 175 and 160 ml/kg for volume (p<0.01) up to day 35, respectively. Chronic lung disease occurred in 12 infants, five of whom were treated with dexamethasone. Artificial ventilation (p<0.01) and dexamethasone treatment (p<0.05) were independent predictors of weight gain. Median weight gain (8.2 and 9.7 g/kg/d), head growth (0.45 and 0.60 cm/week), and LLL growth (0.28 and 0.35 mm/d) were lower (p<0.05) in ventilated than in non-ventilated infants, respectively. The correlation of LLL growth with body length (r=0.31, p<0.05) and head growth (r=0.42, p<0.01) was weak. Dexamethasone arrested growth; median LLL gain was 0.21 and 0.31 mm/d in ventilated infants with and without dexamethasone (p<0.05).
In VLBW infants, fetal growth rates are not reached with current feeding practice. In addition to inadequate nutrition, factors directly related to disease and treatment contribute to postnatal growth failure.
Preterm infants are at risk for suboptimal growth and bone mineralization compared to infants born at term but long-term outcomes into early adulthood are unclear.
To determine (1) if growth and nutrition in the first year of life significantly predict the outcomes measured at adulthood and (2) whole body and regional bone mineral content (BMC) of young adults who were born preterm and weighing <1500 g.
In this descriptive follow-up study, subjects were born preterm and weighing <1500 g (n=25, 17.2+/-1.2 years of age) and originally participated in a 1-year follow-up study of infant growth or subjects born at term (n=25, 17.3+/-1.4 years of age).
In the preterm group, relationships of growth and nutrition in the first year of life with adult anthropometry and BMC were identified using correlation and regression analysis. Birth groups were compared for measurements of anthropometry and whole body and regional BMC obtained at adulthood using t-tests.
After correcting for the effects of bone area using regression, rate of weight gain had a positive relationship and days to regain birth weight a negative relationship to adult BMC. Young adults, born preterm, were significantly shorter with lower whole body BMC than of those born at term, but BMC was appropriate for size.
Growth early in life predicts subsequent attainment of growth and bone mass. Premature birth results in lower attainment of height achieved by young adult age but bone mass is appropriate for body size.
Transmitral flow parameters in preterm and term infants were compared in order to study differences in signal expression and temporal dynamics of left ventricular diastolic function. In 63 preterm infants between 26 and 33 weeks of gestation and 102 term infants, a Doppler survey was performed during 6 months after birth. Early and atrial filling-time velocity integrals and peak velocities were significantly lower in the preterm neonates. Atrial filling parameters reached the level observed in term infants by 2 months of age. Peak early filling velocity was still lower for 2-month-old preterms and attained the term infants' level by 3 months of age. Preterm infants continued having high atrial filling fraction (AFF) (0.51+/-0.07) during 2 months after birth, while in term infants the fraction decreased continuously from 0.41+/-0.06 to 0.37+/-0.05. Isovolumic relaxation time (IVRT) was the only parameter without differences between preterm and term infants, and it decreased from 54+/-7 ms in neonates to 41+/-4 ms over 3 months. Stroke volume passing the mitral valve doubled in preterm (4+/-1 to 7.9+/-1.5 ml/cm2), but increased by only 37% (6.9+/-1.6 to 9.5+/-2.2 ml/cm2) in term infants. Our observations show that the maturational period of diastolic function appears prolonged in preterm infants. As preterm infants have to cope with a higher physiologic preload augmentation during growth, part of the delay in parameter changes might be caused by preload stress rather than by persistence of functional impairment. Although doing well under physiological conditions, preterm neonates may be at higher risk for diastolic dysfunction than term infants when an additional preload challenge is encountered.
Intensive studies have been conducted so far on biochemical markers available for screening of chromosome defects in obstetrical monitoring. In this paper we report further data on two protein phosphatases: alkaline phosphatase (a marker of cell maturation) and phosphotyrosine phosphatase (a marker of cell proliferation) assayed in cultured amniotic cells from fetuses with trisomy 18 at 15 weeks of gestation. Comparison with normal fetal cells showed a different behaviour for each enzyme: alkaline phosphatase was very significantly lowered while phosphotyrosine phosphatase remained a normal levels. These results provide a further enlargement of the field of biochemical markers used in the screening tests of trisomy 18.
It is currently unknown if interleukin (IL)-16 exists in the lungs of ventilated infants, and because the predominant cells in the airways of infants with CLD are CD4+ macrophages, we hypothesized that IL-16 plays a role as a pro-inflammatory mediator in lung inflammation.
To examine if IL-16, a chemoattractant for CD4+ cells, is detectable in airway secretions of ventilated newborns. Its presence may be associated with lung inflammatory responses.
Cohort cross-sectional study.
Thirty-four mechanically ventilated newborn infants.
Tracheal fluid (TF) specimens collected during the first month of life were examined for cell differentials determined from cytospin slides and supernatant was analyzed by ELISA for IL-16.
Eighty-three cross-sectional tracheal fluid (TF) specimens were analyzed. Eleven of the 27 preterm but none of the 7 term infants developed chronic lung disease (CLD). IL-16, ranging from 203 to 42,073 pg/ml, was detected in 16 of the 46 specimens obtained from CLD infants, 1 of the 30 specimens from 16 non-CLD preterm and 2 of the 7 specimens from 7 term infants (p<0.001). Leukocyte counts (median 16.6 vs. 2.0 x 10(-9)/l, p<0.0001) and percentage neutrophils (median 93% vs. 73%, p<0.001) were higher in IL-16 positive specimens.
IL-16 is detectable within the airway secretions of ventilated newborn infants and its presence is associated with a neutrophilic infiltration. Further studies are required to investigate its role in chronic inflammation in CLD.
Preterm children are at risk for behavior problems. Studies examining contributions of intellectual and environmental factors to behavior outcomes in preterm children are mixed.
(1) To identify the nature of maladaptive behaviors in preterm children age 9 to 16 years born across the spectrum of gestational age and birth weight (BW). (2) To examine contributions of BW as a biological factor, socioeconomic status as an environmental factor, and intelligence quotient (IQ) as indicative of intellectual ability to behavior outcomes.
Using the Child Behavior Checklist, parent reports of behavior for 63 preterm children (gestational age 24 to <36 weeks) were compared to 29 full term children of similar age, gender and socioeconomic status. Multiple regression models evaluated effects of prematurity, socioeconomic status, and intellectual ability on behavioral symptom scores.
Preterm children had higher total and internalizing problem scores compared to full term children. They also had lower IQ. BW was a significant predictor of total and internalizing behavior problems. Among the syndrome scales, anxious/depressed and attention problems were elevated. Socioeconomic status did not contribute to behavior scores. IQ contributed to total, but not to internalizing or externalizing, scores. IQ contributed to attention problems, but not to anxious/depressed scores.
Preterm children had increased behavior problems, especially symptoms of inattention and anxiety. Lower BW predicted more behavior problems. IQ acted as a mediator between BW and attention scores, but not anxiety scores. These findings alert health care providers to assess anxiety in all preterm children regardless of intellectual ability and additional study on the influence of intellectual ability on behavioral outcomes in preterm children is needed.
To determine whether proportionate or disproportionate foetal smallness at 17 to 19 weeks of gestation in low-risk pregnancies was associated with size, body constitution, and adverse outcome at birth.
We included ultrasound measurements at 17-19 weeks of gestation in 7285 uncomplicated pregnancies with reliable information on last menstrual period. We considered a foetus with both mean abdominal diameter (MAD) and biparietal diameter (BPD) below the 10th percentile for gestational age, gender, and parity as symmetrically small. Those who had MAD below the 10th percentile and BPD at or above the 10th percentile were asymmetrically small (thin and small).
The occurrence of small for gestational age (SGA) (birth weight below the 10th percentile) decreased with increasing second trimester MAD percentile (P<0.0001). The risk in foetuses which were both thin and extremely small (MAD below the 2.5th percentile) of having weight, ponderal index, crown-heel length, or head circumference below the 10th percentile at birth was 19-28%. The risk of perinatal composite outcome (prenatal death, Apgar score after 5 min < or =7, birth weight below the 10th percentile, or <1500 g, or preterm birth) was 37%. Apgar score of < or =7 at 5 min and explained foetal death both occurred in 7%, which was significantly higher than those with larger MAD.
Asymmetric as well as symmetric foetal smallness may start early in pregnancy. Symmetric and particularly asymmetric small foetuses at 17-19 weeks of gestation were generally lighter, shorter, and thinner at birth and had more often adverse perinatal outcome.
Analysis of comprehensive records over a period of 15 yr permits calculation of the total prevalence of Down Syndrome in an industrial city. The prevalence at birth is shown to have fallen from 1.70 per 1000 births in the period 1961--65 to 0.84 per 1000 births in 1971--75. The fall in prevalence can be shown to be largely due to a change in distribution of maternal age. An earlier increase in the number of Down Syndrome children is shown to reflect a greatly improved survival in the first 5 yr of life to a continuing level of 81%. The number of Down Syndrome children is unlikely to increase much even with increase of birth rate unless older mothers have further pregnancies. For these reasons the policies of amniocentesis of older women and termination of affected pregnancies will have progressively less effect on the number of affected children if this demographic trend continues. A further effect is that special schools will have a proportionately greater burden as the younger children being admitted have less prospect of development and may be more demanding of staff than Down Syndrome children.
Motor development appears to be more affected by premature birth than other developmental domains, however few studies have specifically investigated the development of gross and fine motor skills in this population.
To examine longitudinal motor development in a group of "apparently normal" high-risk infants.
Developmental follow-up clinic in a perinatal centre.
Longitudinal observational cohort study.
Fifty-eight infants born less than 29 weeks gestation and/or 1000 g and without disabilities detected at 12 months.
Longitudinal gross and fine motor skills at 18 months, 3 and 5 years using the Peabody Developmental Motor Scales. The HOME scale provided information of the home environment as a stimulus for development.
A large proportion (54% at 18 months, 47% at 3 years and 64% at 5 years) of children continued to have fine motor deficits from 18 months to 5 years. The proportion of infants with gross motor deficits significantly increased over this period (14%, 33% and 81%, p<0.001), particularly for the 'micropreemies' (born <750 g). In multivariate analyses, gross motor development was positively influenced by the quality of the home environment.
A large proportion of high-risk infants continued to have fine motor deficits, reflecting an underlying problem with fine motor skills. The proportion of infants with gross motor deficits significantly increased, as test demands became more challenging. In addition, the development of gross and fine motor skills appears to be influenced differently by the home environment.
Toxoplasmosis, a zoonosis caused by a protozoan, Toxoplasma gondii, is probably the most widespread human parasitosis in developed countries. Pregnant women with latent toxoplasmosis have seemingly younger fetuses especially in the 16th week of gestation, which suggests that fetuses of Toxoplasma-infected mothers have slower rates of development in the first trimester of pregnancy. In the present retrospective cohort study, we analyzed data on postnatal motor development of infants from 331 questionnaire respondents including 53 Toxoplasma-infected mothers to search for signs of early postnatal development disorders. During the first year of life, a slower postnatal motor development was observed in infants of mothers with latent toxoplasmosis. These infants significantly later developed the ability to control the head position (p=0.039), to roll from supine to prone position (p=0.022) and were slightly later to begin crawling (p=0.059). Our results are compatible with the hypothesis that the difference in the rates of prenatal and early postnatal development between children of Toxoplasma-negative and Toxoplasma-positive mothers might be caused by a decreased stringency of embryo quality control in partly immunosuppressed Toxoplasma-positive mothers resulting in a higher proportion of infants with genetic or developmental disorders in offspring. However, because of relatively low return rate of questionnaires and an associated risk of a sieve effect, our results should be considered as preliminary and performing a large scale prospective study in the future is critically needed.
Serial estimations of maternal urinary oestriol, serum cystine aminopeptidase (S-CAP), and human chorionic somatomammotrophin (S-HCS) were studied prospectively in 29 pregnancies complicated by intrauterine growth retardation. The newborn growth-retarded infants were examined by neurological and behavioural techniques. Growth variables and neurological and developmental findings were compared with those in 18 healthy controls at 5, 10 and 18 months of age. The growth-retarded infants caught up with regard to body size from 5 months of age, although the severely retarded infants (birth weight less than or equal to -2 SD) differed from the controls with regard to weight and head circumference at 18 months of age. Abnormal maternal oestriol excretions were negatively correlated to weight and length during the follow-up period. Infants who had been severely growth-retarded at birth were neurologically below optimal level at 10 months of age, compared to the controls. There were no significant differences between the growth-retarded infants and the controls with regard to psychomotor development, as assessed by a screening test and by Griffiths' method. Significant correlations were found between abnormal biochemical placental tests (especially urinary oestriol and S-CAP) and psychomotor development. Significant correlations also appeared between neonatal orientation and motor behaviour and some Griffiths' scales at 18 months of age. No relationship was found between the neurological condition in the neonatal period and the neurological findings and development at follow-up.
Infants with iron deficiency anemia (IDA) and stunting explore and interact less with their environment. They may also be fatigued more often, suggesting their sleep may be affected. It is unclear whether fatigue in these infants is due to poor nighttime sleep or if it is compensated for with frequent naps or longer sleep.
In 2 studies from Pemba Island, Zanzibar and 1 from Nepal we investigated the relationship between IDA, stunting, and maternal reports of sleep in 6-18 mo old infants.
Parents reported on the number and duration of naps, hours of nighttime sleep, and frequency of night waking. Anemia was defined as Hb<10 g/dL, iron deficiency as zinc protoporphyrin (ZPP > or = 90 micromol/mol heme), stunting as HAZ<-2 SD, and IDA as Hb<10 g/dL and ZPP > or = 90 micromol/mol heme.
The prevalence of IDA and stunting was 34-84% and 22-37%, respectively. Most infants napped during the day and took approximately 1.5 naps (mean nap duration 1.4-1.7 h). Mean nighttime sleep duration was 8.3-9.7 h and infants awoke 2.1-2.5 times per night. Both IDA and stunting were associated with differences in reported sleep characterized by shorter night sleep duration and higher frequency of night waking; stunting was also related to shorter nap duration.
We found reduced sleep duration and increased night waking among infants with IDA and stunting. Because sleep plays an essential role in infant development, our findings indicate a clear need for further research into these relationships.
To determine the effect of prematurity (gestational age (GA) < 32 weeks) on developmental outcome at the corrected age of 18 and 24 months in a regionally defined, prospective cohort study.
The Leiden Follow-Up Project on Prematurity (LFUPP) includes all live-born infants < 32 weeks GA, born in 1996/1997 in three Dutch health regions (n=266). Mental and psychomotor developmental indices (MDI, PDI) were determined with the Bayley Scales of Infant Development I: > or = -1 S.D.: normal, -2 to -1 S.D.: moderate delay and < -2 S.D.: severe delay.
At 18 months 168 (71%) and at 24 months, 151 children (64%) of 235 survivors were assessed. Moderate to severely delayed mental and/or psychomotor development occurred in 40% of the children at both ages. Children lost to follow-up were of lower socioeconomic status and more frequently of non-Dutch origin. Since non-Dutch origin negatively affected the outcome at both test ages, availability of the data of these children would probably have worsened the outcome. Postnatal treatment with dexamethasone was associated with an increased risk of delayed development. Other independent predictors of delayed development were bronchopulmonary dysplasia at 18 months and ethnicity, maternal age at birth, birthweight and gender at 24 months. After adjustment for these other predictors of delayed development, the mean PDI of dexamethasone-treated infants was 16.1 points lower than of non-treated infants at 18 months (p=0.03) and 12.7 points lower at 24 months (p=0.04).
At 18 and 24 months corrected age, 40% of the very prematurely born children had both delayed mental and/or psychomotor development. Treatment with dexamethasone postnatally was a major risk factor for delayed (psychomotor) development.
In this study we examined alpha-fetoprotein (AFP) mRNA expression in fetal liver at 12-15 weeks of gestation in trisomy 21 (n = 13), trisomy 18 (n = 5) and control fetuses (n = 24). No significant difference was found in the steady-state level of fetal liver AFP mRNA levels in either of the two trisomy groups studied. These findings suggest that the decrease in maternal serum AFP concentration found in trisomic pregnancies is unlikely to be the consequence of impaired transcription of the AFP gene by the fetal liver.
To identify important maternal and child factors associated with development of vocabulary in a cohort of children with and without permanent hearing loss (HL).
Children with HL and typical hearing were enrolled after the newborn hearing screen. Mother-child dyads were evaluated at 18-24 months of age. Mothers completed the MacArthur-Bates Communicative Development Inventory (MCDI). Maternal communicative effectiveness was scored using the Parent/Caregiver Involvement Scale (PCIS) from a 10 min play session. Correlations and regression models were run to identify the important predictors of number of child words produced.
Results from 40 children with typical hearing and 31 children with HL are reported. Words produced (134+/-135 vs. 71+/-112) and words produced percentile (33+/-42 vs. 17+/-23) scores on the MCDI were significantly higher for children with hearing compared to children with HL. Greater maternal stress was associated with decreased verbal involvement, positive regard, availability, and enjoyment. Regression analysis revealed HL, stay in a Neonatal Intensive Care Unit (NICU), and maternal stress were associated with fewer words produced whereas more optimal maternal atmosphere and quality of control and directiveness were associated with more words produced.
Maternal communicative behaviors, maternal stress, child HL, and child stay in the NICU were all associated with number of words produced at 18-24 months.
In a long-term prospective study 46 unselected infants born before 35 completed weeks of gestational age were followed up, and compared to 26 fullterm infants. At 9 and 18 months of chronological age their height and weight were still lower than that of fullterms, but the difference disappeared when age was corrected for gestational age at birth. The motor and neurological maturity and language development was delayed in the preterms still at 18 months, which could possibly also be explained by their lower biological age. Ten of the preterm infants showed, at one or several occasions during follow up, definite neurological abnormality. At 18 months of age two of them were handicapped, one with retrolental fibroplasia, nearly blind, and another with cerebral palsy (slight spastic diplegia). Five of them had late psychomotor development, while two were borderline and one normal. We defined pre- and perinatal risk groups, but found that development at 18 months was not correlated to degree of risk. Neither was there any correlation between neurological examination at term and later handicap or psychomotor retardation. We found more illness, mostly due to common infections, during the first 18 months in the preterm group, as measured by the number of visits to a doctor and days spent in hospital.
A cross-sectional study of 64 women and their fetuses undergoing cordocentesis at 18-25 weeks showed no significant correlation between maternal and fetal Hb or MCV and no relationship between these measurements and fetal abdominal circumference. We found no evidence for a nutritional or physiological association between maternal and fetal haematological status.
Preterm infants are recognised as developing at a significantly slower rate than their full-term peers and with different movement quality.
This study aimed to describe the longitudinal gross motor trajectories of these infants in the first 18 months of (corrected) age and investigate factors associated with gross motor development.
A longitudinal study was conducted with convenience samples of 58 preterm infants born < or = 29 weeks of gestation and 52 control full-term infants in Australia.
The infants were assessed at 4, 8, 12 and 18 months of (corrected) age using the Alberta Infant Motor Scale (AIMS).
Forty-six preterm and 48 control infants completed all four assessments. The preterm group scored significantly lower on various sub-scores at all age levels. Almost half of the preterm infants demonstrated less progression in the sit sub-scale from 4 to 8 months (corrected) age, possibly due to an imbalance between flexor and extensor strength in the trunk. At 12 and 18 months of (corrected) age, lack of rotation and fluency in their movements were evident in some preterm infants. Presence of intra-ventricular haemorrhage and chronic lung disease were associated with poor motor performance at 4 months and use of postnatal steroids was associated with poor motor performance at 4, 8 and 18 months of corrected age.
The imbalance between flexor and extensor muscle strength in preterm infants had a stronger impact on motor development than usually expected. The AIMS appears to be a sensitive assessment tool to demonstrate the unique movement characteristics in this preterm cohort.
Very premature infants occasionally have neurodevelopmental disabilities. However, there have been quite limited data on prenatal risk factors associated with their neurodevelopmental outcomes.
To clarify the relationship between prenatal risk factors and neurodevelopmental outcomes of very premature infants.
The study design is a retrospective review.
One hundred seventy Japanese women with a singleton pregnancy and their infants whose birth weight being less than 1500 g were included. We classified those infants into 118 appropriate for gestational age (AGA) and 52 small for gestational age (SGA) infants.
Infants' neurodevelopmental outcomes at 18 months of corrected age were evaluated by the Kyoto Scale of Psychological Development 2001 (KSPD). We analyzed and compared the infants' outcomes and prenatal risk factors between two groups.
Mortality and rate of infants unevaluable by KSPD because of severe impairment were not significantly different between those groups. However, the developmental quotient score of the cognitive-adaptive area in SGA infants born between 25 and 31 weeks of gestation was significantly lower than that in AGA infants randomly selected as gestation-matched controls. More advanced gestational age and heavier birth weight protected against adverse neurodevelopmental outcomes in both groups. Moreover, male infants were related to the excess risk of adverse neurodevelopmental outcomes in the SGA group.
In view of the neurodevelopment of the infants, it seems that the most efficient obstetric strategy for improving prognosis of premature infants should be targeted to prolong the pregnancy period as long as the reassuring fetal status and maternal stable health condition are being confirmed.
The neurological optimality of 418 Dutch children was evaluated at the age of 18 months, in order to determine whether prenatal and breast milk mediated exposure to polychlorinated biphenyls (PCBs) and dioxins affected neurological development. Half of the infants were breast-fed, the other half were formula-fed. PCB concentrations in cord and maternal plasma were used as a measure of prenatal exposure to PCBs. To measure postnatal exposure, PCB and dioxin congeners were determined in human milk and in formula milk. After adjusting for covariates, transplacental PCB exposure was negatively related to the neurological condition at 18 months. Although greater amounts of PCBs and dioxins are transferred via nursing than via placental passage, an effect of lactational exposure to PCBs and dioxins could not be detected. We even found a beneficial effect of breast-feeding on the fluency of movements. We conclude that transplacental PCB passage has a small negative effect on the neurological condition in 18-month-old toddlers.
To determine factors before or at birth that are predictive of growth patterns to 18 months in children born small for gestational age (SGA).
Prospective cohort study of 186 SGA babies. Catch-up growth patterns were defined as early (>10th centile at 6 and 18 months), late (<10th centile at 6 months but >10th centile at 18 months), transient (>10th centile at 6 months but <10th centile at 18 months) or none (<10th centile at 6 and 18 months).
Most children (75%) showed catch-up growth by 6 months. Of antenatal variables studied, only early gestation at diagnosis of SGA predicted late or failed catch-up. Late or failed catch-up was also associated with short gestation, small absolute and relative size at birth, increased placental weight/birthweight ratio (Pl/BW) and prolonged neonatal hospital stay. On logistic regression, both late and failed catch-up were associated with short birth length. Late catch-up growth was also associated with prolonged hospital stay and male sex. Failed catch-up was associated with increased Pl/BW. No antenatal or perinatal variables distinguished early from transient catch-up groups.
SGA babies with late onset and less severe growth restriction have a good chance of catch-up growth by 6 months of age. Catch-up growth is likely to be delayed in SGA babies who are short at birth, are boys, and have prolonged hospital stays. However, poor growth over the first 6 months does not predict later growth patterns. Failure of catch-up growth in babies with increased Pl/BW may reflect an intrinsic growth defect. Transient catch-up growth may reflect environmental factors operating after birth.