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To identify antenatal and intrapartum risk factors associated with seizures in term newborns, 40 infants who had seizures within 72 hours of birth were compared with 400 controls using logistic regression analysis. The risk of seizure in the term newborn was approximately one per 1000 in the population studied. The logistic regression model identified a group of infants in whom the risk of seizure was approximately one per 100. The risk factors included in the model were antepartum anemia, antepartum bleeding, asthma, meconium-stained amniotic fluid, presentation other than occiput anterior, fetal distress, and shoulder dystocia. Consistent with other studies, our analysis confirmed a strong association between seizures and factors that increase the risk of fetal asphyxia.

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Although neonatal intensive care units (NICUs) have contributed to advances in neonatal survival, little is known about the epidemiology of deaths that occur after NICU discharge. To determine mortality rates following NICU discharge, we used linked birth, death, and NICU records for infants born to Georgia residents from 1980 through 1982 and who were admitted to NICUs participating in the state's perinatal care network. Infants who died after discharge (n = 120) had a median duration of NICU hospitalization of 20 days (range, 1 to 148 days) and a median birth weight of 1983 g (range, 793 to 5159 g). The postdischarge mortality rate was 22.7 per 1000 NICU discharges. This rate is more than five times the overall postneonatal mortality rate for Georgia from 1980 to 1982. The most common causes of death were congenital heart disease (23%), sudden infant death syndrome (21%), and infection (13%). Demographic characteristics commonly associated with infant mortality were not strongly associated with the mortality following NICU discharge.

KIE: An examination of linked birth, death, and neonatal intensive care unit (NICU) records for infants born in Georgia from 1980 through 1982 who were admitted to NICUs participating in the state's perinatal care network reveals that infants who died after discharge had a median duration of NICU hospitalization of 20 days and a median birth weight of 1,983 g. The postdischarge mortality rate of 22.7 per 1,000 NICU discharges is more than five times the overall postnatal mortality rate for Georgia from 1980 to 1982. Demographic characteristics associated with infant mortality were not strongly associated with mortality following NICU discharge. The most common causes of death were congenital heart disease, sudden infant death syndrome, and infection.

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This article concerns itself with the effects of HIE on the brain of the full-term infant. Several treatment options are available, with phenobarbital being the drug of choice, but the course remains observation and careful monitoring of the at-risk infant.

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The pseudoreplica method of electron microscopy (EM) was evaluated as a rapid screening technique for the detection of cytomegaloviruria in 3056 neonates in a predominantly lower socioeconomic population. Virus isolation methods detected 49 (1.6%) CMV-positive individuals. When pools of three to five urines were tested, 26 (54%) of the culture-positive neonates were identified by EM; however, testing of individual urines increased EM detection to 33 (67%). Almost all of these urines, as well as urine or oral specimens obtained on follow-up visits, which had infectivity titers greater than or equal to 10(4)/ml were EM-positive, whereas only half of the specimens with titers less than 10(4)/ml were EM-positive. All the symptomatic neonates were detected by EM, suggesting that electron microscopy would be most valuable as a diagnostic aid in this group of CMV-infected neonates.

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In a study population of 151 newborn infants less than 35 weeks gestation, who required intensive care for more than 24 hours, clinical and biochemical factors associated with the presence of intraventricular hemorrhage (IVH) were prospectively evaluated. The diagnosis of IVH was confirmed by computed tomography, ventricular tap, or autopsy. Alveolar rupture was highly correlated with the presence of IVH. Other factors associated with IVH were: hypoxemia, hypercarbia, mechanical ventilation, peak inflation presser > 25 cm H2O, inspiratory to expiratory ratio > 1:1, patent ductus arteriosus, bicarbonate administration after the first day of life, volume expansion in the first day of life, hypotension, stages III and IV hyaline membrane disease, and intrauterine growth retardation. Early bicarbonate administration (first day), sodium administration > 8 mEq/kg/day, acidosis and birth weight less than or equal to 1,200 gm were associated with IVH only in the infants who died with IVH. Factors not associated with IVH were Apgar less than or equal to 5 at one and five minutes, birth weight, gestational age, male sex, osmolality greater than or equal to 300, serum sodium greater than or equal to 150, hypothermia, continuous distending pressure > 6 cm H2O, positive end-expiratory pressure > 5 cm H2O, outborn birth, obstetric trauma, or coagulopathy. Certain therapeutic interventions may lead to an increase incidence of intracerebral hemorrhage in the high-risk preterm infant.

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All neonates with necrotizing enterocoltis cared for at Grady Memorial Hospital from July, 1977, through February, 1979, were compared with controls matched for birth weight and time of admission to the nursery, to examine risk factors which have been implicated in the etiology of the disease. Data on maternal history, birth history, and hospital course were uniformly collected and contrasted for 35 cases and 98 controls. Low birth weight was associated with an increased incidence of NEC and an increased case fatality rate. All babies 36 weeks or more at birth were diagnosed by seven days. More immature infants developed the disease later in their hospital course. In addition, preterm babies who developed NEC after 2 weeks of age appear to be smaller and sicker. Factors previously thought to predispose an infant to the development of the disease, such as prolonged rupture of membranes, infectious complications of pregnancy, low Apgar scores, patent ductus arteriosus, and use of umbilical catheters, were found with equal frequency in cases and controls and may simply represent the descriptive characteristics of a population of sick premature infants. Feeding history and antibiotic use were examined in depth and were not correlated with the development of NEC.

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To determine the incidence of subependymal (SEH) or intraventricular hemorrhage (IVH) and its short-term outcome, infants of less than 35 weeks' gestation who required intensive care were evaluated and computerized tomographic scans obtained. If the scans showed blood, serial scans were followed until the hemorrhage had resolved and ventricle size was stable. Hemorrhage was quantitated; Seventy-seven of 191 (40.3%) infants were shown to have SEH, IVH, or both; 22 of them (28%) died, and hemorrhage was thought to be the primary cause of death in 17. Fifty-five survivors (71%) with SEH, IVH, or a combination of the two had serial follow-up scans. Six had SEH alone; 49 had IVH. Severe progressive hydrocephalus developed in 12 (22%) infants. Thirty-seven (75.5%) die not show progressive hydrocephalus. The degree of hemorrhage in these 37 was mild in 14, moderate in 13, and marked in 10. Of those with progressive hydrocephalus, hemorrhage was marked in 8 and moderate in 4. Hydrocephalus resolved spontaneously in 4 of the 12. Medical treatment (repeated lumbar punctures) was successful in 3, but failed in 4. Hydrocephalus was managed by shunt surgery in 5. This study revealed that the quantity of blood is prognostically important with regard to both survival (p less than 0.001) and development of progressive hydrocephalus (p less than 0.05). Furthermore, hydrocephalus, even if progressive, may not necessitate surgical management;

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Ninety-eight infants of less than 35 weeks' gestation, consecutively admitted to a regional neonatal intensive care unit, were followed prior to computerized tomography (CT) scan for clinical signs of subependymal and/or intraventricular hemorrhage. The presence or absence of intracerebral hemorrhage was confirmed by CT scan in all patients, and the severity of hemorrhage was quantitated as mild, moderate, or marked. Thirty-seven out of 98 infants (38%) demonstrated intracerebral hemorrhage on CT scan; 20 of 37 (54%) were predicted clinically. Clinical predictability was related to severity of hemorrhage as quantitated by CT scan. Clinical signs that were found helpful in predicting subependymal and/or intraventricular hemorrhage were fall in hematocrit, failure of rise in hematocrit with transfusion of packed red blood cells, tight fontanel, decrease in spontaneous activity, decreased tone, abnormal eye signs, and seizures.

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Heart failure in a 2-day-old infant was not readily explained by clinical examination. Cardiac catheterization suggested an intracranial arteriovenous (AV) fistula, and cerebral arteriography showed a malformation of the vein of Galen. The major feeding arteries were surgically obliterated. At age 27 months, the boy has normal mentation but moderate left hemiparesis. Review of the literature disclosed 39 other infants with AV malformations of the vein of Galen producing heart failure before age 3 months. Most of them were boys, and had cyanosis, a systolic murmer, cranial bruit, cardiomegaly, and right bentricular hypertrophy. Only three of the 13 who had surgery for their malformation survived. Removal of the malformation is difficult; obliteration of the nutrient vessels, using the operating microscope, is the currently accepted treatment.

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Seizures, brain swelling, and cortical necrosis have been observed in the newborn rhesus monkey following a 2 to 4-hour period of intrauterine partial asphyxia produced by halothane-induced maternal hypotension. These clinical and neuropathologic findings are similar to those seen in human newborn infants who have experienced an episode of intrauterine asphyxia from such a cause as premature placental separation. The present study strongly indicates that fetal partial asphyxia, from any cause, in the absence of fetal circulatory collapse or fetal head compression, may be the primary event that sets in motion a vicious cycle of brain swelling and impaired cerebral blood flow, leading finally to cerebral necrosis.

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