The value of entry criteria in follow-up clinics for neonatal intensive care unit graduates.

The risk factors used as entry criteria to a service follow-up clinic for a group of neonatal intensive care unit graduates over a 10-year period were compared with neurodevelopmental outcome at one year corrected age. Although most of the individual risk factors did not show significance, two markers associated with the risk factors did: severe encephalopathy and abnormal cranial ultrasound. Of the patients who came for a year, 46% were detected as being abnormal. One-third of the abnormal children weighed more than 1500 g.

Cerebral blood flow velocity in term newborns following intrapartum fetal asphyxia.

Twenty-six term newborns with intrapartum fetal asphyxia, determined biochemically (umbilical artery base deficit > 12 mmol/l), were compared with 59 normal newborns to determine the effect of intrapartum fetal asphyxia on newborn blood pressure and cerebral blood flow velocity following delivery. Cerebral blood flow velocity observations with concurrent measures of blood pressure and heart rate were obtained during the 24 h after delivery and after 24 h. After delivery, diastolic blood pressure in the newborns of the asphyxia group was significantly greater than that of the newborns of the normal group and this difference persisted after 24 h. Cerebral blood flow velocity in the newborns of the asphyxia group was of the same order as that of the newborns of the normal group during the 24 h after delivery. However, there was a significant increase in both peak systolic and end-diastolic blood flow velocity after 24 h. The duration of metabolic acidosis may be a factor in the occurrence of this delayed cerebral blood flow velocity response. Observations of cerebral blood flow velocity should be continued for more than 24 h following delivery to determine the effect of intrapartum fetal asphyxia.

Incidence of neonatal sixth nerve palsy in relation to mode of delivery.

During a 10-year period on a level I neonatal service the total incidence (0.4%) and incidence by mode of delivery of neonatal lateral rectus paralysis occurring among 6886 term neonates was determined. The incidence of abducens nerve injury in this population increased progressively from 0% for deliveries by cesarean section to 0.1% for spontaneous vaginal delivery, to 2.4% for forceps delivery, and to 3.2% for vacuum extraction. This suggests that increased complexity of instrumentation during delivery is associated with an increased risk of sixth nerve palsy. A proposed mechanism for the injury to the sixth nerve is described.

The association between preterm newborn hypotension and hypoxemia and outcome during the first year.

Ninety-eight newborn infants, less than 34 weeks at birth, were studied to examine the relationship between newborn hypotension and hypoxemia and brain damage. Heart rate, blood pressure and oxygen tension were recorded continuously during the 96 h following delivery. Outcome measures included neuropathology in children who died, and motor and cognitive development at one year corrected age in children who survived. There were 22 children with a minor and 27 with a major abnormal outcome. There was a relationship between newborn hypotension, newborn hypoxemia and low birth weight, and a major abnormal outcome. The probability of a major abnormal outcome increased from 8% in newborns with no hypotension or hypoxemia, to 53% in children with both hypotension and hypoxemia. These findings support the contention that combinations of sustained newborn hypotension and hypoxemia are important factors in the development of brain damage, accounting for a major abnormal outcome.

Middle cerebral artery blood flow velocity in the newborn following delivery.

Ninety-five normally grown term and preterm newborns were examined to determine the means and prediction limits of cerebral blood flow velocity following delivery and to examine the relationship of systemic blood pressure to cerebral blood flow velocity. Doppler blood flow velocity was observed during the four days following delivery. Continuous measures of blood pressure and heart rate were recorded concurrently. Mean peak systolic and end diastolic blood flow velocity immediately following delivery was 43.2 and 9.3 cm/sec for term newborn, and 31.8 and 3.3 cm/sec for preterm newborn. During the 24 h following delivery there was no change of peak systolic blood flow velocity but a two to three fold increase of end diastolic blood flow velocity in the term and preterm newborn. The reference limits for peak systolic and end diastolic blood flow velocity provide criteria to define abnormal increases and decreases of blood flow velocity. During the 24 h following delivery, increasing diastolic blood pressure was associated with increasing end diastolic blood flow velocity independent of birth weight and time following delivery. Also there was a significant correlation between systemic pressure pulsatile index and middle cerebral artery blood flow velocity pulsatile index. Thus systemic blood pressure pulsatility must be recognized as distinct from other intracerebral influences on cerebral blood flow velocity regulation in the newborn.

Mortality and morbidity after intrapartum asphyxia in the preterm fetus.

This matched cohort study examined the significance of intrapartum fetal asphyxia determined biochemically in the preterm newborn in regard to outcome during the first year. Thirty preterm newborns with metabolic acidosis at delivery were compared with 60 preterm newborns, matched for birth weight, with normal blood gas measures. Deaths during the first year were reviewed. Assessment of the surviving children at 1 year corrected age included neurologic examination, Bayley scales, and Uzgiris and Hunt scale to define motor and cognitive development. Seven asphyxiated infants (23%) died during the first year compared with two nonasphyxiated infants (3%), a statistically significant difference (P less than .006). Among the surviving children, the incidence of minor motor and/or cognitive deficits was the same in the two groups. The incidence of major motor and/or cognitive deficits in the group with asphyxia (eight of 30) was significantly greater than in the control group (eight of 60) (P less than .03). These results indicate that intrapartum fetal asphyxia in the preterm newborn is a contributing factor to the mortality and morbidity observed in these children.

Hypotension and hypoxemia in the preterm newborn during the four days following delivery identify infants at risk of echosonographically demonstrable cerebral lesions.

This prospective study of 130 preterm newborns at less than 34 weeks gestational age has examined the predictive value of abnormalities in continuously recorded newborn blood pressure, heart rate, and oxygen tension during the 4 d following delivery for echosonographically demonstrable cerebral lesions (EDCL) identified in the infant by six months corrected age. EDCL consisting of intraventricular hemorrhage, ventriculomegaly, or hyperechoic parenchymal lesions in the brain were identified in 44 preterm newborns (34%). The incidence of EDCL in preterm newborns with no hypotension or hypoxemia was 13%. The incidence of EDCL was significantly increased in preterm newborns with either hypotension or hypoxemia. The probability of EDCL exceeded 50% when the total exposure to either hypotension or hypoxemia during the 4 d exceeded 50 mmHg-hours, or when newborn hypotension and hypoxemia occurred concurrently. No relationship to hypertension, bradycardia, or tachycardia was detected. These findings indicate that hypotension and hypoxemia in the preterm newborn during the 4 d following delivery are useful risk markers of EDCL.

Blood pressure and heart rate of the preterm newborn following delivery.

Thirty-five preterm newborns were studied to determine the mean blood pressure and heart rate of preterm newborns less than 1500 gm and greater than or equal to 1500 gm at birth. Systemic blood pressure increased and heart rate decreased with increasing maturity at birth. Both systemic blood pressure and heart rate increased during the four days following delivery. The 95% prediction limits of stable preterm newborns less than 1500 gm and greater than or equal to 1500 gm at birth are useful criteria to define hypertension and hypotension, as well as tachycardia and bradycardia.

The association of fetal and newborn metabolic acidosis with severe periventricular leukomalacia in the preterm newborn.

One hundred twenty preterm newborns less than 34 weeks' gestational age have been studied prospectively to determine the frequency of fetal and newborn metabolic acidosis and to examine the relationship of metabolic acidosis to periventricular leukomalacia as demonstrated by serial newborn ultrasonographic examinations. Fetal metabolic acidosis, based on an umbilical artery buffer base less than 34 mmol/L at delivery, occurred in three cases (2%), one of which had evidence of periventricular leukomalacia. Newborn metabolic acidosis that is based on a buffer base less than 34 mmol/L during the 4 days after delivery occurred in 12 cases (10%), five of which had evidence of periventricular leukomalacia. There is a significant relationship between the degree and duration of newborn metabolic acidosis and the occurrence of periventricular leukomalacia. This study indicates that systemic metabolic acidosis is an important pathophysiologic marker of periventricular leukomalacia. Intrapartum fetal asphyxia with metabolic acidosis, although an infrequent occurrence in the preterm newborn, may account for a few cases of periventricular leukomalacia, while the more common newborn metabolic acidosis, when of sufficient degree and duration, carries a high risk of periventricular leukomalacia.

Motor and cognitive deficits after intrapartum asphyxia in the mature fetus.

The incidence of major and minor motor and/or cognitive deficits at 1 year of age, in 37 mature children who had experienced an intrapartum fetal asphyxial insult, was compared with the incidence of deficits at 1 year in 76 children of the control group. The incidence of both major and minor deficits was significantly greater in the group with intrapartum fetal asphyxia in relation to the control group. These findings support the concept that, beyond a critical threshold of fetal asphyxia, a continuum of casualty in the surviving newborn infants exists.

Motor and cognitive development of infants with intraventricular hemorrhage, ventriculomegaly, or periventricular parenchymal lesions.

Two hundred twenty-six moderate- or high-risk newborn infants were studied to examine the relationship between ultrasound findings in the newborn period and at 6 months and motor and cognitive deficits at 1 year. A three-part classification of abnormal ultrasound findings was used to grade intraventricular hemorrhage, ventriculomegaly, and parenchymal lesions. Abnormal ultrasound findings were observed in 48 infants, of whom 21 had intraventricular hemorrhage, 18 persistent ventriculomegaly, and nine parenchymal lesions. The incidence of deficits was as follows: normal ultrasound examination, 20%; intraventricular hemorrhage, 33%; persistent ventriculomegaly, 67%; and parenchymal lesions, 89%. The present study indicates that serial ultrasound examinations are indicated in preterm newborn infants less than 1500 gm and in selected newborn infants at risk and greater than 1500 gm at birth. The three-part classification of abnormal ultrasound findings should be used because of the predictive significance of persistent ventriculomegaly and parenchymal lesions for motor and cognitive deficits at 1 year of age.

Maternal, fetal, and newborn complications associated with newborn intracranial hemorrhage.

Two hundred twenty newborn infants with one or more fetal or newborn complications and 54 newborn infants without fetal or newborn complications were prospectively studied to assess the relationship between maternal, obstetric, fetal, and newborn complications and intracranial hemorrhage. Intracranial hemorrhage occurred in 47 newborn infants with fetal or newborn complications (21%) and in one infant with no fetal or newborn complications (2%). Maternal and obstetric complications, duration of labor, and mode of delivery were not associated with intracranial hemorrhage. Newborn immaturity at delivery is an important factor in the occurrence of intracranial hemorrhage. There is little evidence that fetal hypoxia is a contributing factor. Severe respiratory complications and major infections are newborn complications associated with intracranial hemorrhage.

The contribution of fetal-newborn complications to motor and cognitive deficits.

A total of 364 selected high-risk premature and mature infants were studied prospectively to assess the relationship between fetal-newborn complications and motor and cognitive deficits identified during the first year of life. Deficits occurred in 24 per cent of the children: 14 per cent had one or more major deficit and the other 10 per cent had one or more minor deficit. Prematurity was one of the fetal-newborn complications not associated with deficits at one year. Complications that were associated with deficits included fetal hypoxia, respiratory difficulties, infection and newborn encephalopathy. There was also a significant association between fetal hypoxia, newborn respiratory complications, infection and newborn encephalopathy, which is in keeping with the concept that the first three may be mechanisms in CNS injury and subsequent deficits, while newborn encephalopathy reflects the injury and is an important predictor of such deficits.

The relationship between perinatal hypoxia and newborn encephalopathy.

Newborn encephalopathy was observed in 30% of 303 selected high-risk preterm and term newborn infants. The newborn encephalopathy was mild or moderate in 65 children and severe in 27. The predictive significance of newborn encephalopathy to motor and cognitive deficits at 1 year was evident from the incidence of deficits in the children with no encephalopathy (17%), in children with mild or moderate encephalopathy (25%), and in children with severe encephalopathy (55%). The biologic risk factors with a significant association with newborn encephalopathy included severe intrapartum fetal hypoxia, moderate and severe newborn respiratory complications, and major infections. Perinatal hypoxia was associated with, and may have contributed to, 26% of the cases of mild and moderate newborn encephalopathy and 66% of the cases of severe newborn encephalopathy. Fetal and newborn hypoxia occurred with equal frequencies in cases of mild and moderate encephalopathy; however, newborn hypoxia was twice as frequent as fetal hypoxia in cases of severe newborn encephalopathy.

Factors associated with motor and cognitive deficits in children after intrapartum fetal hypoxia.

Sixty children with biochemical evidence of intrapartum fetal hypoxia were studied to define the factors which distinguish the children with deficits from those without deficits of motor and cognitive development. Follow-up assessment included growth measures, neurological examination, Bayley Scales of Infant Development, and a modified Uzgiris and Hunt Scale. Eight children (13%) had a major deficit and 10 children (16%) had a minor deficit at 1 year. Children with deficits had an episode of hypoxia that was more severe and prolonged and, subsequent to delivery, a greater incidence of severe respiratory complications, apnea, and newborn encephalopathy. No other significant risk factors were identified. It is concluded that an episode of hypoxia less than one hour may occur without subsequent deficits. However, an episode of hypoxia in excess of 1 hour resulting in a metabolic acidosis of the order of 25 mEq/L will be followed by motor and cognitive deficits in approximately 50% of children.

The predictive significance of biologic risk factors for deficits in children of a high-risk population.

Two hundred forty-two high-risk children and 47 low-risk children were prospectively studied to assess the relationship between biologic risk factors that occurred during the perinatal period and the motor and cognitive deficits that were identified during the first year of life. Multiple risk factors were present in 80% of the children of the high-risk group. Provisional deficits were classified on the degree of abnormality found in a clinical and behavioral assessment that included neurological examinations, Bayley Physical and Mental Development Scales, and the Uzgiris and Hunt Scale. Provisional deficits occurred in 10% of the children of the low-risk group. High-risk children had a significantly greater incidence of provisional deficits, particularly in respect to positive deficits. In high-risk children, the probability of a deficit was 17% in those without infection or encephalopathy, 30% in those with infection, and 40% in those with encephalopathy.

Intrapartum fetal hypoxia: a study of long-term morbidity.

Reported is the second phase of a prospective follow-up study of 37 children who had episodes of intrapartum fetal hypoxia at delivery identified by an acid-base assessment and of a control group of 59 children who had no evidence of intrapartum fetal hypoxia. The newborn infants were normally grown and mature at delivery. Follow-up assessments of motor, cognitive, and language development were made between 1 and 6 years of age. There was no significant difference in the pattern of physical growth and the incidences of motor and cognitive handicap or developmental delay, language developmental delay, and tests of vision and hearing in the children of the hypoxia group and the children of the control group. These findings suggest that acid-base measures of metabolic acidosis can be used as a method of assessment of the mature normally grown fetus during labor without compromising the long-term outcome of the child.

Intrauterine growth retardation: a study of long-term morbidity.

Reported is the second phase of a prospective follow-up study of 76 growth-retarded children who were mature at birth and a control group of 88 children who had weights appropriate for gestational age at birth. Follow-up assessments of motor, cognitive, and language development were made between 1 and 6 years of age. The children of the intrauterine growth retardation (IUGR) group continued to be smaller than the children of the control group between 12 and 60 months of age. There was no significant difference in the incidences of motor and cognitive handicap or developmental delay, language developmental delay, and tests of vision and hearing between the children of the IUGR group and the children of the control group. There was no significant differences in performance in senior kindergarten between the children of the IUGR group and those of the control group. There was a significant relationship between the socioeconomic status, as measured by the Blishen score at birth, and the subsequent occurrence of motor and cognitive deficits.

The clinical prediction of intrauterine growth retardation.

From a total study group of 8,030 deliveries, 2,788 patients with risk factors and 292 representative patients from the 5,242 patients without risk factors were selected for detailed analysis of predictors of intrauterine growth retardation (IUGR). Two thirds of the IUGR infants came from the population with risk factors and a weighting was assigned to individual risk factors. One third of the IUGR infants came from the population without risk factors, and their mothers demonstrated significantly differing maternal characteristics from those with a normally grown infant. The perinatal mortality rate was higher in the IUGR group and particularly in the population with risk factors.

Intrapartum fetal asphyxia: a preliminary report in regard to long-term morbidity.

This is a preliminary report of a prospective follow-up study of 42 infants who had episodes of intrapartum fetal asphyxia at delivery identified by an acid-base assessment and a control group of 69 babies who had no evidence of intrapartum fetal asphyxia. The newborn infants were mature at delivery. There were no major neurologic disabilities in the asphyxia group. The pattern of physical growth and the mental and physical development indices of the babies of the asphyxia group were similar to those of the control group babies at 12 months of age. Results have not as yet indicated that the mature fetus with at least a terminal episode of asphyxia will exhibit evidence of handicap due to central nervous system injury.