We studied whether changes in cerebral blood-flow velocity occur during the respiratory-distress syndrome and whether, if present, they are related to the subsequent occurrence of intraventricular hemorrhage. Fifty infants weighing less than 1500 g at birth who required mechanical ventilation for the respiratory-distress syndrome were studied from the first hours of life. Blood-flow velocity in the anterior cerebral artery was measured at the anterior fontanel by means of the Doppler technique. At 12 hours of age, the infants had blood-flow velocity patterns that were either stable or fluctuating and that reflected the patterns of simultaneously recorded blood pressure. Intraventricular hemorrhage subsequently developed in 21 of 23 infants with the fluctuating pattern (in most of them, within the next 24 hours), but in only 7 of 27 infants with the stable pattern. Preliminary data suggest that the cerebral hemodynamic fluctuations are related to the respiratory disease and particularly to the mechanics of respiration. We conclude that the fluctuating pattern of cerebral blood-flow velocity in infants with the respiratory-distress syndrome indicates an extreme risk of the development of intraventricular hemorrhage and may represent a major and potentially preventable etiologic factor.
Younger age at presentation, administration of more than two doses of benzodiazepines and deviation from the CSE protocol appear to be factors which influence admission of children to ICU. Recognition of pre-hospital administration of benzodiazepines and adherence to therapeutic guidelines may reduce the need for ventilatory support in this group.
The incidence of periventricular-intraventricular hemorrhage (PV-IVH) in a group of 460 preterm infants with birth weight less than 2,250 gm, studied by cranial ultrasonography, was 39%. Sixty-four (36%) of the infants with periventricular-intraventricular hemorrhage had, in addition, periventricular intraparenchymal echodensity (IPE) evident on ultrasound scan. Thirty-three of the 64 infants had large IPE, and 31 had small IPE. Large IPE consisted of globular echodensity, most often on the side of maximum intraventricular hemorrhage, extending from the external angle of the lateral ventricle into major portions of the white matter of the frontal and parietal lobes; small IPE, often bilateral, consisted of linear echodensity extending for a few millimeters from the external angle of the lateral ventricle into the periventricular white matter. The outcome for infants with large and small IPE differed markedly. Mortality was greatest (94%) for infants with large IPE and birth weight less than 1,000 gm. All survivors with large IPE, regardless of birth weight, had moderate to severe neurological deficits evident on follow-up. In contrast, infants with small IPE and birth weight less than 1,000 gm had a mortality of 38%. Moreover, 70% of all survivors with small IPE were free of neurological deficits on follow-up. The difference in outcome appeared to relate in largest part to the severity of the parenchymal involvement. These data have major significance for decisions concerning management of infants with periventricular-intraventricular hemorrhage and intraparenchymal involvement.
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