51 research outputs found
A Model Analysis of Arterial Oxygen Desaturation during Apnea in Preterm Infants
Rapid arterial O2 desaturation during apnea in the preterm infant has obvious clinical implications but to date no adequate explanation for why it exists. Understanding the factors influencing the rate of arterial O2 desaturation during apnea () is complicated by the non-linear O2 dissociation curve, falling pulmonary O2 uptake, and by the fact that O2 desaturation is biphasic, exhibiting a rapid phase (stage 1) followed by a slower phase when severe desaturation develops (stage 2). Using a mathematical model incorporating pulmonary uptake dynamics, we found that elevated metabolic O2 consumption accelerates throughout the entire desaturation process. By contrast, the remaining factors have a restricted temporal influence: low pre-apneic alveolar causes an early onset of desaturation, but thereafter has little impact; reduced lung volume, hemoglobin content or cardiac output, accelerates during stage 1, and finally, total blood O2 capacity (blood volume and hemoglobin content) alone determines during stage 2. Preterm infants with elevated metabolic rate, respiratory depression, low lung volume, impaired cardiac reserve, anemia, or hypovolemia, are at risk for rapid and profound apneic hypoxemia. Our insights provide a basic physiological framework that may guide clinical interpretation and design of interventions for preventing sudden apneic hypoxemia
Permissive tolerance of the patent ductus arteriosus may increase the risk of Chronic Lung Disease
Joseph W Kaempf,1 Robert Huston,2 YingXing Wu,1 Andrew J Kaempf,1 Lian Wang,1 Gary Grunkemeier,1 Rebecca Mischel,2 Howard Cohen,3 Bret Freitag41Providence St Vincent Medical Center, Portland, OR, 2Randall Children’s Hospital at Legacy Emanuel, Portland, OR, 3Salem Hospital, Salem, OR, 4Legacy Salmon Creek Hospital, Vancouver, WA, USAPurpose: Because early closure therapies of the patent ductus arteriosus (PDA) have not been shown to confer benefit to premature infants, the authors’ four neonatal intensive care units adopted a less aggressive PDA management protocol.Study design: A before–after investigation in infants with PDAs born 501–1500 g. Era 1 (January 2005 to December 2007) featured traditional management with indomethacin and/or surgical ligation used early to close PDAs; Era 2 (January 2008 to June 2009) featured fluid restriction and watchful waiting for PDA closure, limiting indomethacin or surgical ligation to only those infants with large PDAs needing significant respiratory support.Results: Era 2 infants (n = 129, mean ± standard deviation 27 ± 2 weeks) received less and later indomethacin and less Day 1–28 total fluids as compared to Era 1 infants (n = 240, mean ± standard deviation 27 ± 2 weeks). The Chronic Lung Disease (CLD) rate was higher in Era 2 (48% versus 34%, P < 0.01) as was the combined outcome of Death after Day 7 or CLD (57% versus 42%, P < 0.01). Multiple regression analysis showed Era 2 birth was a predictor of CLD. However, Poisson regression analysis determined the predictors of all seven major Vermont Oxford Network morbidities were earlier gestational age, lower birth weight, and male gender, not the era of birth. Significantly more infants were discharged home with PDAs in Era 2.Conclusion: Permissive tolerance of PDAs may increase the risk of CLD and Death after Day 7 or CLD but is not associated with significant changes in other Vermont Oxford Network morbidities.Keywords: premature infant, indomethacin, surgical ligation, quality improvemen
Managing aggression and violence: The clinician’s role in contemporary mental health care
Outcomes of 23- and 24-weeks gestation infants in Wellington, New Zealand: A single centre experience
Optimal perinatal care of infants born less than 24 weeks gestation remains contentious due to uncertainty about the long-term neurodevelopment of resuscitated infants. Our aim was to determine the short-term mortality and major morbidity outcomes from a cohort of inborn infants born at 23 and 24 weeks gestation and to assess if these parameters differed significantly between infants born at 23 vs. 24 weeks gestation. We report survival rates at 2-year follow-up of 22/38 (58%) at 23 weeks gestation and 36/60 (60%) at 24 weeks gestation. Neuroanatomical injury at the time of discharge (IVH ≥ Grade 3 and/or PVL) occurred in in 3/23 (13%) and 1/40 (3%) of surviving 23 and 24 weeks gestation infants respectively. Rates of disability at 2 years corrected postnatal age were not different between infants born at 23 and 24 weeks gestation. We show evidence that with maximal perinatal care in a tertiary setting it is possible to achieve comparable rates of survival free of significant neuroanatomical injury or severe disability at age 2 in infants born at 23-week and 24-weeks gestation
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