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To determine mean arterial pressure values during the first 24 hours for \"stable\" and \"unstable\" extremely low birth weight (ELBW) infants and to ascertain its association with perinatal factors. In ELBW infants, hypotension is diagnosed by nonspecific clinical signs together with reference arterial pressure values extrapolated from regression models or from scarce actual observations. Retrospective cohort study. 101 ELBW (< or = 600 g) infants born in our medical center (1989-2000). Considered stable were 36 infants with umbilical cord hemoglobin > or = 14 g/dl who, although mechanically ventilated, had normal acid-base balance, no patent ductus arteriosus, had not received indomethacin, steroids, muscle relaxants, narcotics, were never treated for hypotension and survived at least 7 days. The remaining 65 infants constituted the unstable group. Arterial pressures were determined by oscillometry (OBP) and direct transducer readings through an umbilical line (MAP). All admission and 10% of the readings were by OBP; the remaining 1877 measurements were by MAP. Stable and unstable infants were similar in birth weight, demographics, history of chorioamnionitis, antepartum steroids, low Apgar scores, administration of epinephrine during resuscitation, and sepsis. Stable infants were different from unstable in gestational age (27+/-2 vs 25+/-2 weeks' gestational age [w GA]), history of preterm labor, preeclampsia, and neonatal mortality (22 vs 68%). Admission OBP (30+/-7 vs 29+/-10 Torr) were similar and 1-hour MAP were different (30+/-6 vs 27+/-7 Torr) between both groups. MAP for stable infants was higher throughout the 24 hours. Greater differences were noted between 3 and 6 hours when 34 of 65 unstable infants were treated for hypotension. Mean MAP and 10 percentile values for stable infants at 1, 3, 6, 12, and 24 hours were 30 (22), 31 (24), 32 (25), 34 (24), and 35 (28) Torr, respectively. MAPs did not correlate with birth weight, but they were lower among 19 stable infants < or = 26 w GA than among 17 stable infants > or = 27 w GA. History of preeclampsia, antenatal steroids, intratracheal epinephrine and cord hemoglobin did not influence MAP. Low 1-minute Apgar score and intracranial hemorrhage were associated with low MAP during the first day. There is a wide variation of GA among ELBW infants. MAPs increase with GA and with postnatal age. Shortly after birth, arterial pressures are similar for stable and unstable infants. Failure to increase MAP between 3 and 6 hours of life should create concern. MAP < or = 28 Torr at 3 hours of life is a reasonable, but not absolute, predictor of the need for hypotension treatment.

Importance Meta-analyses suggest that corticosteroids may be associated with increased survival without cerebral palsy in infants at high risk of bronchopulmonary dysplasia (BPD) but are associated with adverse neurologic outcomes in low-risk infants. Whether this association exists in contemporary practice is uncertain because most randomized clinical trials administered corticosteroids earlier and at higher doses than currently recommended. Objective To evaluate whether the pretreatment risk of death or grade 2 or 3 BPD at 36 weeks’ postmenstrual age modified the association between postnatal corticosteroid therapy and death or disability at 2 years’ corrected age in extremely preterm infants. Design, Setting, and Participants This cohort study analyzed data on 482 matched pairs of infants from 45 participating US hospitals in the National Institute of Child Health and Human Development Neonatal Research Network Generic Database (GDB). Infants were included in the cohort if they were born at less than 27 weeks’ gestation between April 1, 2011, and March 31, 2017; survived the first 7 postnatal days; and had 2-year death or developmental follow-up data collected between January 2013 and December 2019. Corticosteroid-treated infants were propensity score matched with untreated controls. Data were analyzed from September 1, 2019, to November 30, 2022. Exposure Systemic corticosteroid therapy to prevent BPD that was initiated between day 8 and day 42 after birth. Main Outcomes and Measures The primary outcome was death or moderate to severe neurodevelopmental impairment at 2 years’ corrected age. The secondary outcome was death or moderate to severe cerebral palsy at 2 years’ corrected age. Results A total of 482 matched pairs of infants (mean [SD] gestational age, 24.1 [1.1] weeks]; 270 males [56.0%]) were included from 656 corticosteroid-treated infants and 2796 potential controls. Most treated infants (363 [75.3%]) received dexamethasone. The risk of death or disability associated with corticosteroid therapy was inversely associated with the estimated pretreatment probability of death or grade 2 or 3 BPD. The risk difference for death or neurodevelopmental impairment associated with corticosteroids decreased by 2.7% (95% CI, 1.9%-3.5%) for each 10% increase in the pretreatment risk of death or grade 2 or 3 BPD. This risk transitioned from estimated net harm to benefit when the pretreatment risk of death or grade 2 or 3 BPD exceeded 53% (95% CI, 44%-61%). For death or cerebral palsy, the risk difference decreased by 3.6% (95% CI, 2.9%-4.4%) for each 10% increase in the risk of death or grade 2 or 3 BPD and transitioned from estimated net harm to benefit at a pretreatment risk of 40% (95% CI, 33%-46%). Conclusions and Relevance Results of this study suggested that corticosteroids were associated with a reduced risk of death or disability in infants at moderate to high pretreatment risk of death or grade 2 or 3 BPD but with possible harm in infants at lower risk.