Physiology of transition from intrauterine to extrauterine life
ABSTRACT The transition from fetus to newborn is the most complex adaptation that occurs in human experience. Lung adaptation requires coordinated clearance of fetal lung fluid, surfactant secretion, and onset of consistent breathing. The cardiovascular response requires striking changes in blood flow, pressures, and pulmonary vasodilation. Energy metabolism and thermoregulation must be quickly controlled. The primary mediators that prepare the fetus for birth and support the multiorgan transition are cortisol and catecholamine. Abnormalities in adaptation are frequently found following preterm birth or cesarean delivery at term, and many of these infants need delivery room resuscitation to assist in this transition.
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- "Altogether these factors will predispose preterm infants to respiratory insufficiency and the need for positive pressure ventilation and oxygen supplementation. In this scenario, the achievement of a stable pre-ductal SpO 2 is substantially delayed even in healthy well-adapted preterm infants  . Recently, a group of researchers developed a SpO 2 reference range for the first ten minutes after birth for term and preterm infants who did not receive any medical intervention in the delivery room. "
ABSTRACT: Premature infants often experience difficulties adapting to postnatal life. The most relevant ones are related to establishing an adult type cardiorespiratory circulation and acquiring hemodynamic stability, aerating the lung and attaining a functional residual capacity, performing an adequate gas exchange and switching to an oxygen enriched metabolism, and keeping an adequate body temperature. In recent years a body of evidence supports a trend towards gentle management in the delivery room aiming to reduce damage especially to the lungs in the so-called first golden minutes. Herewith, we describe and update four of the most relevant interventions performed in the delivery room: delayed cord clamping, non-invasive ventilation, individualized oxygen supplementation, and maintaining an adequate body temperature so as to avoid hyperthermia and/or hypothermia. Copyright © 2015 Elsevier Ltd. All rights reserved.Paediatric Respiratory Reviews 03/2015; DOI:10.1016/j.prrv.2015.02.004 · 2.22 Impact Factor
- NeoReviews 06/2012; 13(6):e334-e335. DOI:10.1542/neo.13-6-e334
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ABSTRACT: Very low birth weight preterm newborns are susceptible to the development of debilitating inflammatory diseases, many of which are associated with chorioamnionitis. To define the effects of chorioamnionitis on the fetal immune system, IL-1b was administered intra-amniotically at ∼80% gestation in rhesus monkeys. IL-1b caused histological chorioamnionitis, as well as lung inflammation (infiltration of neutrophils or monocytes in the fetal airways). There were large increases in multiple proinflammatory cytokine mRNAs in the lungs at 24 h postadministration, which remained elevated relative to controls at 72 h. Intra-amniotic IL-1b also induced the sustained expression of the surfactant proteins in the lungs. Importantly, IL-1b significantly altered the balance between inflammatory and regulatory T cells. Twenty-four hours after IL-1b injection, the frequency of CD3+CD4+FOXP3+ T cells was decreased in lymphoid organs. In contrast, IL-17A–producing cells (CD3+CD4+, CD3+CD42, and CD32CD42 subsets) were increased in lymphoid organs. The frequency of IFN-g–expressing cells did not change. In this model of a single exposure to an inflammatory trigger, CD3+CD4+FOXP3+ cells rebounded quickly, and their frequency was increased at 72 h compared with controls. IL-17 expression was also transient. Interestingly, the T cell profile alteration was confined to the lymphoid organs and not to circulating fetal T cells. Together, these results suggest that the chorioamnionitis-induced IL-1/IL-17 axis is involved in the severe inflammation that can develop in preterm newborns. Boosting regulatory T cells and/or controlling IL-17 may provide a means to ameliorate these abnormalities.The Journal of Immunology 06/2013; 191(3). DOI:10.4049/jimmunol.1300270 · 5.36 Impact Factor