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OBJECTIVE: To determine whether preterm children born at

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We developed a nursery Neurobiologic Risk Score (NBRS) based on potential mechanisms of brain cell injury in preterm infants and correlated it with developmental outcome at the corrected ages of 6, 15, and 24 months. The NBRS was determined at 2 weeks of age and at the time of discharge from intensive care in 58 preterm infants with birth weights less than or equal to 1500 gm. The NBRS correlated significantly with the Bayley Scales of Infant Development, Mental Development Index (MDI) (r = -0.61 to -0.40) and Psychomotor Development Index (PDI) (r = -0.59 to -0.46), and with abnormal neurologic examination findings (r = 0.59 to 0.73) at the three testing periods. Although 12 of the 13 items composing the NBRS individually correlated with one or more outcome variables, seven items (infection, blood pH, seizures, intraventricular hemorrhage, assisted ventilation, periventricular leukomalacia, and hypoglycemia) accounted for almost all of the explained variance. Logistic regression of individual items demonstrated intraventricular hemorrhage to be the most important item for predicting the MDI at 24 months; pH was the most influential item for predicting the PDI at every testing period. A shorter, revised NBRS that included only the seven significant items demonstrated as strong a correlation with developmental outcome as the original NBRS. A revised 2-week score of greater than or equal to 5 or a discharge score of greater than or equal to 6 demonstrated 100% specificity and had a 100% positive predictive value for an abnormal outcome at 24 months of age in this group of infants. We conclude that the NBRS identifies during the intensive care nursery stay those infants at highest risk for an abnormal outcome related to nursery events. In addition, analysis of NBRS items provides insight into the relative importance of individual factors for influencing mental, motor, and neurologic outcome.

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To determine if crying alters cerebral hemodynamics and oxidative metabolism in the brain, near infrared spectrophotometry was used to assess relative changes in cerebral blood volume and the oxidation-reduction state of cytochrome aa3. Thirty-six crying episodes were observed, 20 in healthy infants and 16 in infants with respiratory problems. Throughout all crying episodes cerebral blood volume and oxidized cytochrome aa3 demonstrated oscillatory fluctuations every 10 to 20 seconds, with maximum changes during prolonged exhalations. In 86% of episodes baseline blood volume rose and remained elevated during the cry. The relative content of deoxyhemoglobin in cerebral blood also rose, indicating that venous blood is the major contributor to the increase in blood volume. Changes in baseline cytochrome aa3 oxidation varied with the presence of lung disease and with the chronologic age of the infant. Cytochrome reduction with crying occurred significantly more often in infants with respiratory problems than in healthy infants. Cytochrome aa3 became more oxidized in 82% of crying episodes in healthy infants older than 3 days of age, but no change in cytochrome oxidation was usually noted in those younger than 3 days. Thus crying alters cerebral blood volume in all neonates in a pattern consistent with cyclic obstruction to cerebral venous return; it decreases cerebral oxygenation in infants with respiratory problems.

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Relative changes in cerebral blood volume and in the oxidation/reduction state of cytochrome aa3, the terminal member of the electron transport chain in oxidative metabolism, can be simultaneously observed with near infrared spectroscopy. Using this technique, we studied movement-associated blood pressure elevations in three nonparalyzed very low birth weight infants receiving mechanical ventilation. We defined hypertensive peaks as increases in systolic and diastolic blood pressures greater than or equal to 30% over baseline and lasting at least 2 seconds. Ninety percent of monitored time, an increase in tissue blood volume (tBV) immediately followed each blood pressure elevation, with deoxygenated hemoglobin providing the sole or predominant increase in tBV. A simultaneous shift of cytochrome aa3 to a more reduced state usually accompanied the rise in tBV, probably indicating a transient imbalance between oxygen delivery and cellular oxygen utilization and a failure of mechanisms that normally regulate cerebral oxygenation. The consistent association of hypertensive peaks with body movement, coughing, and breath holding, and the predominant increase in deoxygenated hemoglobin suggest that increased intrathoracic pressure transiently impedes cerebral venous return. The repeated fluctuations in intracerebral blood volume and associated shifts to greater cytochrome aa3 reduction with hypertensive peaks provide a possible explanation for the association of fluctuating blood pressure patterns and increased risk for intraventricular hemorrhage.

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The effects on the neonate of severe maternal hypertension originating before the thirty-sixth week of gestation were determined by comparing data obtained on 28 preterm infants born of hypertensive mothers with data from 28 gestational age-matched controls. All hypertensive mothers had diastolic blood pressure greater than or equal to 110 mm Hg, proteinuria, and systemic symptoms of their disease; over half had thrombocytopenia and significant elevations of LDH and SGOT. All hypertensive mothers had been treated intravenously with magnesium sulfate, and 79% received other antihypertensive agents. When compared to control infants, the infants of hypertensive mothers had a significantly higher incidence of somatic growth retardation, microcephaly, thrombocytopenia, leukopenia, neutropenia, low Apgar scores, delayed adaptation, patent ductus arteriosus, hypotonia, and gastrointestinal hypomotility. Apgar scores, platelet count, WBC count, neutrophil count, and weight percentile correlated with the severity of maternal platelet and enzyme abnormalities. The occurrence of gastrointestinal hypomotility, hypotonia, and patent ductus arteriosus may be related to transplacental passage of maternally administered drugs.

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Forty preterm infants with maternal isoxsuprine exposure less than 24 hours delivery and 40 matched control infants were studied prospectively to determine the acute neonatal effects of maternal ISX exposure. The cord ISX concentration correlated inversely with the drug-free interval before delivery (P < 0.001). Cord ISX concentrations > 10 mg/ml were seen only with intravenous maternal therapy and a drug-discontinuance to delivery interval of two hours or less. The plasma half-life of ISX in neonates ranged from 1.7 to 8 hours; gestationally younger infants required a longer time for drug clearance. Ileus was 13 times more common in the ISX group and was not directly related to the cord ISX concentration. The incidence of hypotension and hypocalcemia rose directly with the cord ISX concentration, reaching 89% and 100%, respectively, when the cord ISX level exceeded 10 ng/ml. The incidence of respiratory distress syndrome was low in the ISX infants with low cord drug values, but increased to that of the control group when the cord ISX concentration reached > 10 ng/ml.

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A retrospective study of all inborn infants at 26 to 35 weeks' gestational age delivered from August, 1976, through July, 1977, was undertaken to determine the effects on the neonate of maternal isoxsuprine therapy for premature labor. Mothers of 43 infants received ISX within 48 hours of delivery and mothers of 107 received no ISX. Hypocalcemia, hypoglycemia, evidence of ileus, hypotension, and neonatal death were all significantly more common in infants whose mothers received ISX. Hypotension and death occurred predominantly in infants of 26 to 31 weeks' gestation and in infants whose mothers developed hypotension or tachycardia during ISX infusion. The frequency of hypotension and death decreased as the time interval from the loading dose of ISX to delivery increased.

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