Survival and major neonatal complications in infants born between 22 0/7 and 24 6/7 weeks gestation (1999–2003)
This study was undertaken to compare survival and morbidity until discharge in infants born after 22-23 versus 24 weeks' gestational age (GA).
Cohort study of all infants 25 weeks or less, born in 3 tertiary perinatal centers (1999-2003).
Of a total of 336 infants, 133 (40%) died before or immediately after birth without the provision of life support, 203 (60%) received active neonatal treatment. Infants with life support (n = 82 at 22 to 23 weeks, n = 121 at 24 weeks) differed with respect to antenatal steroid prophylaxis (44% vs 62%) and cesarean section rate (51% vs 71%). Survival was 67% compared with 82% (P = .016). The incidence of intraventricular hemorrhage III or greater or periventricular leukomalacia (15/15%), severe retinopathy of prematurity (18/15%), and chronic lung disease (40/47%) was similar in both GA groups.
The provision of life support for extremely preterm infants increases their chance of survival without more neonatal morbidity.
Available from: Sandra Horsch
Available from: Frans J Walther
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ABSTRACT: Advances in pharmacology and technology have pushed back the limits of viability to 23−24 weeks of gestation at the expense of an increasing number of survivors with disabilities. Treatment of these extremely preterm infants should be based on a thorough determination of diagnosis and prognosis, followed by decision-making on the basis of futility of treatment or quality-of-life issues and the counselling of parents. This paper reviews the survival rates and outcome of infants under 26 weeks of gestation born in Europe and the rest of the world, and discusses the role of parents and the influence of condition at birth, gender and birth weight on ethical decision-making on behalf of these infants. Dutch guidelines on the treatment of extremely preterm infants at birth are presented to assist clinicians facing the challenging ethical, moral, legal and emotional dilemmas that surround this hot topic in perinatology.
Available from: ajplung.physiology.org
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ABSTRACT: Many extremely preterm infants continue to suffer from bronchopulmonary dysplasia, which results from abnormal saccular-stage lung development. Here, we show that fibroblast growth factor-10 (FGF-10) is required for saccular lung development and reduced in the lung tissue of infants with bronchopulmonary dysplasia. Although exposure to bacteria increases the risk of bronchopulmonary dysplasia, no molecular target has been identified connecting inflammatory stimuli and abnormal lung development. In an experimental mouse model of saccular lung development, activation of Toll-like receptor 2 (TLR2) or Toll-like receptor 4 (TLR4) inhibited FGF-10 expression, leading to abnormal saccular airway morphogenesis. In addition, Toll-mediated FGF-10 inhibition disrupted the normal positioning of myofibroblasts around saccular airways, similar to the mislocalization of myofibroblasts seen in patients with bronchopulmonary dysplasia. Reduced FGF-10 expression may therefore link the innate immune system and impaired lung development in bronchopulmonary dysplasia.
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