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OBJECTIVE: In piglets prolonged asphyxia resulted in decreased cerebrospinal fluid (CSF) 3;,5;-cyclic adenosine monophosphate (cAMP) during recovery; this was associated with reduced pial arteriolar responses to stimuli that use cAMP as a second messenger. We hypothesized that asphyxia in human neonates results in decreased CSF cAMP and that low CSF cAMP is associated with abnormal outcome. DESIGN: We studied 27 infants with evidence of hypoxic-ischemic insult; 19 were term (group 1) and 8 were preterm (group 2). The normal values of CSF cAMP were determined from 75 infants with no asphyxia; 44 were term (group 3) and 31 were preterm (group 4). CSF cAMP was measured by using radioimmunoassay procedures. RESULTS: CSF cAMP levels in infants with asphyxia (groups 1 and 2) were 12 +/- 9. 5 and 7.9 +/- 7.1 pmol/mL, respectively, significantly lower than those of groups 3 and 4 (control infants), that is, 21.1 +/- 8.7 and 27.1 +/- 9.2 pmol/mL, respectively (P <.0001). Among infants with asphyxia, 3 died and 10 had abnormal neurologic outcome. Univariate analysis showed that abnormal outcomes were significantly related to CSF cAMP levels, phenobarbital use, and multi-organ failure. However, only CSF cAMP was retained in the model by stepwise logistic regression. CSF cAMP of 10.0 pmol/mL discriminated between those with normal and those with abnormal neurologic outcome. Low CSF cAMP concentration was associated with abnormal long-term outcome, estimated odds ratio of 12.4 (95% CI, 2.1-109.3; P <.006), and sensitivity, specificity, and positive and negative predictive values of 85%, 69%, 73%, and 80%, respectively. CONCLUSION: CSF cAMP concentrations were decreased in infants with asphyxia. Low CSF cAMP levels were associated with poor neurologic outcome.

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We determined the cerebral hemodynamic changes in infants with asymptomatic polycythemic hyperviscosity syndrome and whether treatment with partial plasma exchange transfusion (PPET) would affect hemodynamics as well as outcome. From a routine cord blood hematocrit screening, 71 babies were identified as needing to be tested for polycythemic hyperviscosity. In addition to clinical evaluation, each infant had radial artery hematocrit and viscosity determinations, blood gas determinations, cerebral blood flow velocity studies, cranial ultrasonography, and noninvasive intracranial pressure determination. Babies with symptomatic hyperviscosity (n = 17) were treated by PPET, whereas those with asymptomatic hyperviscosity (n = 28) were randomly selected to have PPET (n = 14) or to be observed (n = 14). The remaining babies (n = 26) with normal viscosity served as control subjects. Both hematocrit and viscosity decreased after PPET but remained unchanged in babies with hyperviscosity who were merely observed. Reversal of cerebral blood flow velocity abnormalities was observed after PPET in the infants with symptomatic hyperviscosity, whereas those who had no symptoms had normal results on Doppler studies at the outset, and no significant changes occurred with either PPET or observation. There were two deaths in the group with symptoms. A total of 46 babies returned for follow-up evaluation at a mean age of 30 +/- 7.7 months. Outcome of the control group was no better than that of those who had hyperviscosity, and outcomes did not differ between the babies with symptomatic and those with asymptomatic hyperviscosity, nor between those treated with PPET and those who were only observed. Multivariate analysis revealed that other perinatal risk factors and race rather than polycythemia or PPET, significantly influenced long-term outcome.

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Bedside microcomputer-derived, minute-to-minute mean arterial pressure (MAP) values during the first 48 hours of life were studied in 100 preterm babies with birth weight less than or equal to 1500 gm. In those babies (n = 72) with no periventricular-intraventricular hemorrhage (PV-IVH) or with grade 1 PV-IVH, the MAP values increased during the study period, with minute-to-minute variation and interval undulation. The MAP values in those with birth weight greater than 1000 gm were higher than in those of lower birth weight. Infants in whom grades 2 to 4 PV-IVH developed (n = 28) had consistently lower MAP values during the study period. Minute-to-minute variability, expressed as the average of the coefficients of variation at 15-minute intervals, did not differ between birth weight groups, nor did they differ between the PV-IVH group and their matched control subjects. However, those with PV-IVH spent a greater percentage of time, with a coefficient of variation greater than or equal to 13% or less than 3%, than their matched control subjects spent (p less than 0.005). This study provides reference data for MAP changes in premature babies. The observed MAP changes in those with PV-IVH lend support to a significant role for MAP alterations in the pathogenesis of PV-IVH.

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The association between periventricular-intraventricular hemorrhage (PV-IVH) and frequent handling resulting from various neonatal intensive care procedures and routine interventions was evaluated in a prospective clinical study. Inborn premature babies with birth weight less than or equal to 1500 gm (n = 156) who did not have PV-IVH or who had grade 1 PV-IVH at less than or equal to 1 hour were randomly assigned to the reduced manipulation protocol (n = 62) or to standard care (n = 94). A bedside microcomputer-based data acquisition system was used to monitor the duration of rest or the number of interventions per day. Infants assigned to receive reduced manipulation spent a significantly higher percentage of time each day at rest than did those who received standard manipulation (p less than 0.006). However, the incidence of grades 2 to 4 PV-IVH did not differ significantly (30% in the study vs 37% in the standard manipulation group). When we analyzed the effect of manipulation in relation to risk of PV-IVH, while taking into account other perinatal variables, standard manipulation was not associated with increased risk of grades 2 to 4 PV-IVH. However, low birth weight, maternal smoking, general anesthesia, early grade 1 PV-IVH, low hematocrit, lowest arterial oxygen pressure within the first 6 hours of life, and large base deficit at 6 hours of age all increased the relative risk of grades 2 to 4 PV-IVH.

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A prospective, random selection, double-blind clinical trial was carried out to determine the efficacy of indomethacin in preventing periventricular-intraventricular hemorrhage (PV-IVH). Babies who were born in our institution, had birth weights less than or equal to 1500 gm, and had no PV-IVH or grade 1 PV-IVH were given either placebo (n = 70) or indomethacin (n = 71), 0.2 mg/kg intravenously at 6 hours of age and 0.1 mg/kg at 18 and 30 hours. Two major outcomes were determined: the development of grades 2 to 4 PV-IVH and the development of severe PV-IVH (i.e., hemorrhages with blood filling greater than 50% of the ventricles and in some cases with associated parenchymal echodensities). Grades 2 to 4 PV-IVH occurred in 16 (23%) of the indomethacin group and 27 (39%) of the placebo group (p less than 0.03). The incidence of severe PV-IVH was 3% in the indomethacin-treated babies and 14% in the control group (p less than 0.02). The influence of other perinatal factors on the incidence of grades 2 to 4 or severe PV-IVH was determined by stepwise logistic regression. Placebo use, early grade 1 PV-IVH, lower birth weight, and higher fraction of inspired oxygen at 6 hours of life were associated with higher estimated odds of the development of grades 2 to 4 PV-IVH. Placebo use, male gender, lower 5-minute Apgar score, and a large base deficit were predictive of severe PV-IVH. Estimated odds ratios of severe PV-IVH with placebo use and male gender were 11.25:1 and 9:1, respectively. Thus indomethacin prophylaxis reduced the relative risk of grades 2 to 4 PV-IVH and severe PV-IVH, but other perinatal variables contributed significantly to the overall risk of PV-IVH.

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We examined the clinical significance of noninvasive intracranial pressure measurements and pulsatility indices in 74 infants with confirmed IC-IVh. The intracranial pressure measurements were obtained using the applanation principle, and the pulsatility indices were calculated from the Doppler flow velocity tracings of the anterior cerebral artery. Fifty-three infants (71.6%) who died had a significantly lower birth weight and gestational age than those who survived. Survival rate decreased significantly with increased intracranial pressure (P less than 0.0002) and increased pulsatility indices (P less than 0.0001). We found no significant relationship between outcome and the size of IC-IVH demonstrated by CT scan. Birth weight, intracranial pressure measurements, and cerebral arterial pulsatile flow changes appear to be major prognostic indicators in neonatal IC-IVH.

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Simultaneous blood and saliva samples were drawn for determination of caffeine and theophylline concentrations in 17 infants receiving caffeine or theophylline therapy for apnea of prematurity. The relationship between serum and saliva concentrations in each drug treatment group was explored using (1) regression analysis and (2) serum:saliva ratio. Significant correlations were observed between serum and salivary concentrations. Salivary concentrations approximated 76 to 80% of the serum concentrations based on the derived serum:saliva ratios. When salivary concentrations were less than 8 microgram/ml, the serum concentrations did not exceed therapeutic range and no clinical toxicity was noted. Monitoring of salivary drug concentrations as an alternative to serum drug concentrations may be useful in preterm infants on methylxanthine therapy. When salivary concentrations exceed 8 microgram/ml, serum concentrations should be determined.

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The cerebrovascular hemodynamic alterations in asphyxia and intracerebral-intraventricular hemorrhage were determined by monitoring the pulsatile flow changes in the anterior cerebral arteries using Doppler ultrasound. The pulsatility index measurements, which were calculated from the recorded changes in Doppler frequency shifts, were obtained in four groups of newborn infants with the following diagnoses: Group I--normal term (n=21); Group II--asphyxia (n=12); Group III--IC-IVH (n=14); and Group IV--asymptomatic preterm (n=11). There was no significant difference between PI values of Groups I and IV. Compared to normal term infants, those diagnosed as having asphyxia had significantly lower PI measurements and those with IC-IVH had significantly higher PI values than the asymptomatic pretern infants. Serial Doppler studies were also performed in 22 preterm infants with respiratory distress. One-half of these infants subsequently developed IC-IVH. Prior to hemorrhage, their PI measurements were significantly lower than those who did not eventually have the complication. The low PI values in asphyxia and prior to the onset of IC-IVH indicate vasodilation and decreased resistance to blood flow. In IC-IVH, the high PI measurements denote the opposite. In infants with respiratory distress in the presence of significant vasodilation and lowered vascular resistance, CBF may increase to excessive levels, resulting in IC-IVH.

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