Objectives:To construct and validate a model and derive a simple rule that is usable in any birth location for the prediction of outcome of term infants with severe asphyxia. Design:Retrospective cohort study. Setting...Objectives:To construct and validate a model and derive a simple rule that is usable in any birth location for the prediction of outcome of term infants with severe asphyxia. Design:Retrospective cohort study. Setting:Regional outborn neonatal intensive care unit. Participants:Infants with postintrapartum asphyxial hypoxic-ischemic encephalopathy (n = 375). Main Exposures:Clinical and laboratory predictors available at age 4 hours. Main Outcome Measures:A logistic regression model was developed and internally validated (with random sampling and based on the year of birth) for severe adverse outcome,which was defined as death or severe disability (severe cerebral palsy,severe developmental delay,sensorineural deafness,or cortical blindness singly or in com bination). A simple prediction rule was derived from 3 variables. Results:Complete data were available for 302 (92%) of the 345 infants with known outcomes (204 infants with severe adverse outcome). Six independent predictors of outcomes were identified. Using the 3 most significant predictors (chest compressions,age at onset of respiration,and base deficit),severe adverse outcome rates were 46%(95%confidence interval,33%-58%) with none of the 3 predictors,64%(95%confidence interval,54%-73%) with any 1 predictor,76%(95%confidence interval,66%-85%)with any 2 predictors,and 93%(95%confidence interval,81%-99%)-with all of the 3 predictors present. The internal validations revealed a robust model. Conclusions:This predictive model for neonatal hypoxic-ischemic encephalopathy provides a sliding scale of probabilities that could be used for prognostication and to design eligibility criteria for decision making including neuroprotective therapy.展开更多
Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to b rain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. Objective: To determine whether hyperoxa...Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to b rain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. Objective: To determine whether hyperoxaemia and/or hypocapnia during the first 2 hours of life add to the risk of brain injury after intrapar tum asphyxia. Methods: Retrospective cohort study in term infants with post-asp hyxial hypoxic ischaemic encephalopathy (HIE) born between 1985 and 1995.Severe and moderate hyperoxaemia were defined as PaO2 > 26.6 and PaO2 > 13.3 kPa (20 0 and 100 mm Hg). Severe and moderate hypocapnia were defined as PaCO2 < 2.6 an d PaCO2 < 3.3 kPa (20 and 25 mm Hg). Adverse outcome ascertained by age 24 mont hs was defined as death, severe cerebral palsy, or any cerebral palsy with blind ness, deafness, or developmental delay. With outcome as the dependent variable, multivariate analyses were performed including hyperoxaemic and hypocapnic varia bles, and factors adjusted for initial disease severity. Results: Of 244 infants , 218 had known outcomes, 127 of which were adverse (64 deaths, 63 neurodevelopm ental deficits). Multivariate analyses showed an association between adverse out come and episodes of severe hyperoxaemia (odds ratio (OR) 3.85, 95%confidence interval (Cl) 1.67 to 8.88, p = 0.002), and severe hypocapnia (OR 2.34, 95% Cl 1.02 to 5.37, p = 0.044). The risk of adverse outcome was highest in infan ts who had both severe hyperoxaemia and severe hypocapnia (OR 4.56, 95%Cl 1.4 to 14.9, p = 0.012). Conclusion s: Severe hyperoxaemia and severe hypocapnia were associated with adverse outcom e in infantswith post-asphyxial HIE. During the first hours of life, oxygen sup plementation and ventilation should be rigorously controlled.展开更多
文摘Objectives:To construct and validate a model and derive a simple rule that is usable in any birth location for the prediction of outcome of term infants with severe asphyxia. Design:Retrospective cohort study. Setting:Regional outborn neonatal intensive care unit. Participants:Infants with postintrapartum asphyxial hypoxic-ischemic encephalopathy (n = 375). Main Exposures:Clinical and laboratory predictors available at age 4 hours. Main Outcome Measures:A logistic regression model was developed and internally validated (with random sampling and based on the year of birth) for severe adverse outcome,which was defined as death or severe disability (severe cerebral palsy,severe developmental delay,sensorineural deafness,or cortical blindness singly or in com bination). A simple prediction rule was derived from 3 variables. Results:Complete data were available for 302 (92%) of the 345 infants with known outcomes (204 infants with severe adverse outcome). Six independent predictors of outcomes were identified. Using the 3 most significant predictors (chest compressions,age at onset of respiration,and base deficit),severe adverse outcome rates were 46%(95%confidence interval,33%-58%) with none of the 3 predictors,64%(95%confidence interval,54%-73%) with any 1 predictor,76%(95%confidence interval,66%-85%)with any 2 predictors,and 93%(95%confidence interval,81%-99%)-with all of the 3 predictors present. The internal validations revealed a robust model. Conclusions:This predictive model for neonatal hypoxic-ischemic encephalopathy provides a sliding scale of probabilities that could be used for prognostication and to design eligibility criteria for decision making including neuroprotective therapy.
文摘Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to b rain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. Objective: To determine whether hyperoxaemia and/or hypocapnia during the first 2 hours of life add to the risk of brain injury after intrapar tum asphyxia. Methods: Retrospective cohort study in term infants with post-asp hyxial hypoxic ischaemic encephalopathy (HIE) born between 1985 and 1995.Severe and moderate hyperoxaemia were defined as PaO2 > 26.6 and PaO2 > 13.3 kPa (20 0 and 100 mm Hg). Severe and moderate hypocapnia were defined as PaCO2 < 2.6 an d PaCO2 < 3.3 kPa (20 and 25 mm Hg). Adverse outcome ascertained by age 24 mont hs was defined as death, severe cerebral palsy, or any cerebral palsy with blind ness, deafness, or developmental delay. With outcome as the dependent variable, multivariate analyses were performed including hyperoxaemic and hypocapnic varia bles, and factors adjusted for initial disease severity. Results: Of 244 infants , 218 had known outcomes, 127 of which were adverse (64 deaths, 63 neurodevelopm ental deficits). Multivariate analyses showed an association between adverse out come and episodes of severe hyperoxaemia (odds ratio (OR) 3.85, 95%confidence interval (Cl) 1.67 to 8.88, p = 0.002), and severe hypocapnia (OR 2.34, 95% Cl 1.02 to 5.37, p = 0.044). The risk of adverse outcome was highest in infan ts who had both severe hyperoxaemia and severe hypocapnia (OR 4.56, 95%Cl 1.4 to 14.9, p = 0.012). Conclusion s: Severe hyperoxaemia and severe hypocapnia were associated with adverse outcom e in infantswith post-asphyxial HIE. During the first hours of life, oxygen sup plementation and ventilation should be rigorously controlled.
