EEG and long-term outcome of term infants with neonatal hypoxic-ischemic encephalopathy.

OBJECTIVE: The prognostic value of a burst suppression pattern (BSP) on the electroencephalograph (EEG) in the prediction of long-term outcome for full term newborns with hypoxic-ischemic encephalopathy (HIE) is well established. The purpose of our study was to compare the patterns of burst suppression on EEG with long-term neurological outcome in term infants with HIE. METHODS: We retrospectively analyzed all records of all full-term newborn infants born at the University of Alberta Hospital between January 1, 1991 and December 31, 1992, who had clinical evidence of HIE and had at least one EEG during the first week of life. The EEGs were reviewed and blindly subclassified into a BSP, or if the pattern was not continuous or was incomplete, a modified burst suppression pattern (MBSP), based on specified electrophysiological criteria. The long-term neurological outcome was then correlated with the EEG pattern. RESULTS: Twenty-three full-term infants were studied. Fifteen had a BSP on EEG and 8 had a MBSP. Six of 15 infants with a BSP died. Of the 9 survivors with a BSP, 7 are disabled and two are normal. Of the 8 infants in the MBSP group, one infant died, two are disabled and 5 are normal. In the BSP group, 6/7 disabled infants developed cerebral palsy while in the MBSP group, only one developed cerebral palsy. CONCLUSION: The results are suggestive of a better outcome for infants with neonatal HIE and MBSP on EEG compared with those with a BSP. Subclassification of the EEG changes of neonatal HIE into BSP and MBSP may give a more accurate prediction of outcome in perinatal asphyxia and assist in discussion with parents about prognosis.

Rescue high frequency oscillatory ventilation for preterm infants: neurodevelopmental outcome and its prediction.

The role of rescue high-frequency oscillatory ventilation (HFO) in treating very-low-birth-weight neonates with severe respiratory failure in relation to neurodevelopmental outcome has not been evaluated. We performed a retrospective cohort study on 21 patients (out of 52 consecutively admitted preterm neonates with gestational age < or = 30 weeks and birth weight < or = 1.250 g; mortality rate 60%) rescued with HFO between October 1988 and August 1993. Neurodevelopment, including Bayley Scales in Infant Development, was assessed at 12-61 (mean 28.5) months adjusted age. Thirteen normal (scores better than 2 SD below mean, and no sensory or motor disability) (62%) and neurodevelopmentally disabled children (38%) survived more than 1 year for developmental assessment. The mental and performance developmental indices were 94 (78-117) and 89 (68-110), and 63 (49-102) and 49 for the 13 normal and 8 disabled children, respectively (both p < 0.05). The incidence of bronchopulmonary dysplasia, intraventricular hemorrhage (IVH; grade 3 or 4), growth retardation, developmental scores and disabilities of these 21 HFO survivors were not significantly different from that of a birth-weight- and gestational-age-matched comparison group. While all HFO survivors had significant improvement in oxygenation 12 and 24 h after starting HFO, FiO2 and the alveolar-arterial oxygen gradient (A-aDO2) decreased significantly 1 h after starting HFO in survivors with normal neurodevelopmental outcome. The lack of initial response to HFO (20% decrease in A-aDO2 1 h after starting HFO) and the presence of grade 3 or 4 IVH predicted neurodevelopmental disability with a sensitivity of 63%, a specificity of 100%, and positive and negative predictive values of 100 and 81%, respectively. We concluded that HFO could be used as a rescue treatment in sick preterm neonates. The lack of early improvement in oxygenation and the presence of grade 3 or 4 IVH can predict adverse early childhood neurodevelopment in such neonates.

Pulmonary vascular resistance during lipid infusion in neonates.

Using two-dimensional echocardiography, pulmonary vascular resistance was estimated from right ventricular pre-ejection period to ejection time (RVPEP/ET) in 11 preterm infants with respiratory distress, to test the effect of different doses of continuous lipid infusion. Echocardiography was performed at baseline with no lipid infusing 2 and 24 hours after 1.5 and 3 g/kg/day of intravenous lipid, 24 hours after discontinuing intravenous lipid emulsion, and 2 hours after restarting intravenous lipid. After 24 hours of intravenous lipid at 1.5 g/kg/day the RVPEP/ET rose to mean (SD) 0.287 (0.03) from a baseline value of 0.225 (0.02) and to 0.326 (0.05) after 24 hours of intravenous lipid at 3 g/kg/day. Pulmonary arterial pressure returned to baseline 24 hours after the intravenous lipid had been discontinued. Continuous 24 hour infusion of lipid caused significant dose and time-dependent increases in pulmonary vascular resistance. Intravenous lipid may aggravate pulmonary hypertension.

Early versus late onset neonatal septicemia at Children's Hospital.

An analysis was made of 695 cases of neonatal sepsis at Children's Hospital from 1982 to 1986. The incidence of neonatal sepsis and septicemia were 6.5 and 2.4 per 1,000 livebirths respectively. There were 178 cases of septicemia with onset during the first four days of life (early onset group) and 77 cases with onset after four days of life (late onset group). Both groups did not differ significantly in sex, birth weight and gestational age. Most of the cases had low birth weight and were premature. Pneumonia was the common associated infection. Omphalitis was found more frequently in the early onset of septicemia, whereas, NEC and skin infection were found more in the late onset group. Pseudomonas aeruginosa and Klebsiella pneumoniae were the major causes of infection in both groups. Staphylococcus was more common in late septicemia. No statistical difference in major complications was found between the two groups. Fatality rate in early and late septicemia was 32.6 and 28.2 per cent respectively.

Perinatal mortality at Children's and Rajvithi Hospitals in 1983-1987.

In the period between 1983-1987, there were 101,056 births at Rajvithi hospital. Out of these, 6,158 sick newborn were transferred to Children's hospital for further care. The incidence of low birth-weight infants was 9.42 per cent. Average perinatal mortality was 14.49 per 1,000 births, ranging from 13.44 to 15.52 per 1,000 births. The major causes of early neonatal death were perinatal asphyxia, respiratory distress syndrome (RDS), immaturity (less than 1,000 g), congenital anomalies, and infection. Beyond this period (7-28 days of age) the causes of death were infection, congenital anomalies, bronchopulmonary dysplasia, necrotizing enterocolitis, apnea and others. Asphyxia and RDS are still the major causes of death that could be further reduced.

PIP: This study reveals the perinatal and neonatal mortality between 1983 and 1987 at Children's and Rajvithi Hospitals, Bangkok, Thailand, and the causes of death with the leading early neonatal (END) cause being asphyxia and respiratory distress syndrome (RDS). The late neonatal (7-28 days) and the post natal cause was infection. A decline in perinatal mortality from 28/1,000 births in 1978 to 13.7 in 1987 was due to 1980 improvements in obstetrics and early neonatal care, reflecting a general trend in decreasing perinatal mortality. There was no major cause of late fetal death, however one-third were macerated, and 15% of stillbirths were congenital anomalies including over 60% from anencephaly and other central nervous system defects. 101,056 births were recorded at Rajvithi with Children's Hospital transfers of those who were sick or weighed less than 2000 grams. 9.42% were low birth weight with males more than females. 30% died within the first 24 hours of life. Mortality was 14.49/1000 births. 4.67% of ENDs were low birthweight, while only .19 for a full-sized infant. The author attributed quality of care at Children's and the low socioeconomic (SES) status of the population to the presence of sepsis and nocosomial infections and asphyxia and RDS. Ramathibodi Hospital with better care and a higher SES reports the leading cause of death between 1979 and 1983 as congenital anomalies; death due to asphyxia and RDS is no longer a significant cause of death. The author urges better prenatal care and hospital conditions.