To summarize the literature on mortality rates and prevalences of major neurodevelopmental disabilities and to examine trends of these outcomes over time in extremely premature neonates. Data Sources: MEDLINE was used to search the English literature for studies published since 1970 reporting on both mortality and disability in infants born at or before 26 weeks' gestation (extremely immature [EI] cohort), with a birth weight of 800 g or less (extremely small [ES] cohort), or subgroups of these. Study Selection: Studies were included in the analysis if all of the following were reported: mortality; direct examination of 75% or more of the survivors; and the proportion of patients with at least 1 of the following disabilities: cerebral palsy, mental retardation, blindness, and deafness. Studies reporting cohorts included as a subset of cohorts in another study were excluded. Forty-two studies providing mortality and disability data for 20 cohorts of 4116 EI infants and 38 cohorts of 4345 ES infants born after 1972 met the inclusion criteria. Data Extraction: Data were abstracted from all studies that met these criteria by two of us (J.M.L. and D.E.W.), independently; the data were then cross-checked to ensure accuracy. Results: Survival averaged 41% for EI infants and 30% for ES infants, and it increased significantly with time. In contrast to mortality, the prevalences of major neurodevelopmental disabilities among survivors have not changed over time. The most common major disability was mental retardation, found in 14% of EI and ES survivors. Cerebral palsy was found in 12% of EI survivors and 8% of ES survivors, blindness was found in 8% of EI and ES survivors, and deafness was found in 3% of EI and ES survivors. Overall, 22% of EI survivors and 24% of ES survivors were classified as having at least 1 major disability. Each 100 EI or ES livebirths yielded 7 children with major disabilities; this prevalence was correlated with survival across cohorts. Conclusions: The prevalence of disabilities had not changed among EI or ES survivors with increasing survival. However, increasing survival of these infants has resulted in a steadily increasing prevalence of children with disabilities.
Ventilatory management patterns in very low birth weight newborns, particularly iatrogenic hypocapnia, have occasionally been implicated in perinatal brain damage. However, such relationships have not been explored in large representative populations. To examine the risk of disabling cerebral palsy in mechanically ventilated very low birth weight infants in relation to hypocapnia and other ventilation-related variables, we conducted a population-based prospective cohort study of 1105 newborns with birth weights of 500 -2000 g born in New Jersey from mid-1984 through 1987, among whom 777 of 902 survivors (86%) had at least one neurodevelopmental assessment at age 2 y or older. Six hundred fifty-seven of 777 assessed survivors (85%), of whom 400 had been mechanically ventilated, had blood gases obtained during the neonatal period. Hypocapnia was defined as the highest quintile of cumulative exposure to arterial PCO 2 levels Ͻ35 mm Hg during the neonatal period. Disabling cerebral palsy was diagnosed in six of 257 unventilated newborns (2.3%), 30 of 320 ventilated newborns without hypocapnia (9.4%), and 22 of 80 ventilated newborns with hypocapnia (27.5%). Two additional ventilatory risk factors for disabling cerebral palsy were found-hyperoxia and prolonged duration of ventilation. In a multivariate analysis, each of the three ventilatory variables independently contributed a 2-to 3-fold increase in risk of disabling cerebral palsy. These risks were additive. Although duration of mechanical ventilation in very low birth weight newborns likely represents severity of illness, both hypocapnia and hyperoxia are largely controlled by ventilatory practice. Avoidance of arterial PCO 2 levels Ͻ35 mm Hg and arterial PO 2 levels Ͼ60 mm Hg in mechanically ventilated very low birth weight infants would seem prudent. The successes of neonatal intensive care during the past two decades in reducing neonatal mortality have not been matched by success in reducing the risk of CP and other neurodevelopmental disorders. The population prevalence of CP has changed little in developed countries during the past three decades (1-7).CP has generally been thought to be caused by antepartum or intrapartum factors. But some recent studies in low birth weight infants have focused on the relationship of components of neonatal intensive care, particularly the management of mechanical ventilation, as risk factors for brain damage. Several studies have pointed to the possibility that the iatrogenic induction of hypocapnia (low PaCO 2 ) might cause brain damage, mediated via the well-established effects of hypocapnia in decreasing CBF. Under normal circumstances, a direct monotonic relationship between CBF and PaCO 2 and an inverse relationship of CBF to PaO 2 provide a compensatory mechanism through which hypoxemia or hypercapnia can provoke cerebral vasodilation. However, under circumstances of artificial hypocapnia or hyperoxemia the same mechanism could result in an inappropriate reduction in CBF.Although some neonatologists try to avoid hypoc...
Near universal initiation of intensive care in NJ, compared with selective initiation of intensive care in NETH, was associated with 24.1 additional survivors per 100 live births, 7.2 additional cases of DCP per 100 live births, and a cost of 1372 additional ventilator days per 100 live births.
ABSTRACT. Objectives. We tested the hypothesis that administration of magnesium sulfate in labor protects against the development of neonatal brain lesions and cerebral palsy (CP) in low birth weight infants.Methods. Magnesium exposure was ascertained in a population-based cohort of 1105 infants weighing 2000 g or less through review of medical records of maternal magnesium sulfate administration and, where available, elevated maternal serum magnesium levels. Neonatal germinal matrix/intraventricular hemorrhage and parenchymal brain lesions were ascertained by a prospective, timed ultrasound scanning protocol in the first week of life. CP was ascertained at 2 years of age by clinical examination in 80% of survivors and by interview and medical record review in another 6% and was classified as disabling or nondisabling. Conclusions. The hypothesis that magnesium sulfate use reduces the risk of neonatal brain lesions or CP in low birth weight infants was not statistically supported in this study, although a modest reduction in risk of DCP cannot be excluded. The data further suggest that magnesium exposure may be associated with reduction in risk of CP in low birth weight infants who have lateonset brain lesions, but this unpredicted observation requires confirmation in another data set. Pediatrics 1997; 99(5). URL: http://www.pediatrics.org/cgi/content/full/99/ 5/e1; cerebral palsy; magnesium sulfate; infant, low birth weight; preeclampsia; cerebral hemorrhage, infant. Results. No significant reduction in risk of nondisabling CP (adjusted odds ratio [OR
We address the issue of statistical power and sample size for cost-effectiveness studies. Tests of hypotheses on the cost-effectiveness ratio (CER) are constructed from the net cost and incremental effectiveness measures. When the difference in effectiveness is known, we derive formulae for statistical power and sample size assessments for one- and two-sided tests of hypotheses of the CER. We also construct a test of the joint hypothesis of cost-effectiveness and effectiveness and derive an expression connecting power and sample size. Our methods account for the correlation between cost and effectiveness and lead to smaller sample size requirements than comparative methods that ignore the correlation. The implications of our formulae for cost-effectiveness studies are illustrated through numerical examples. When compared with trials designed to demonstrate effectiveness alone, our results indicate that a trial appropriately powered to demonstrate cost-effectiveness might require sample sizes many times greater.
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