Hyperoxia in Very Preterm Infants

Johns Hopkins University and the Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19107, USA.
The Journal of perinatal & neonatal nursing (Impact Factor: 1.1). 07/2011; 25(3):268-74. DOI: 10.1097/JPN.0b013e318226ee2c
Source: PubMed


Supplemental oxygen plays a critical role in the management of infants born at the lower limit of viability, but not without the risk of complications resulting from high levels or prolonged exposure. Longitudinal studies of very premature infants, born at less than 28 weeks' gestation, establish a clear relationship between pulse oximetry saturation readings above 92%, or hyperoxia, and development of severe retinopathy of prematurity, chronic lung disease, and brain injury. Hyperoxia is neither natural nor random. It is an unintended consequence of intervention. A comprehensive review of the literature reveals a strong association between exposure to hyperoxia and subsequent expression of comorbidities. Owing to this knowledge, eradication of hyperoxia, and consequent reduction of sequelae, is a significant public health concern that deserves attention by the neonatal community. Although prospective, collaborative meta-analyses will soon provide needed additional data to inform practice, existing compelling evidence supports urgent practice change to reduce exposure to hyperoxia in very preterm infants.

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    • "Hyperoxic ventilation is frequently involved in neonatal intensive care units for treatment of respiratory distress syndrome and pulmonary hypertension. However, many authors recommend limitation of hyperoxia exposure in the newborn period due to increased awareness about its noxious effects [1]–[3]. Premature newborns, in particular, are known to be more susceptible to oxidative stress due to immaturity of the antioxidant system [4]–[5] and due to deficiency of antioxidant precursors in parenteral nutrition [6]. "
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    ABSTRACT: Premature newborns are frequently exposed to hyperoxic conditions and experimental data indicate modulation of liver metabolism by hyperoxia in the first postnatal period. Conversely, nothing is known about possible modulation of growth factors and signaling molecules involved in other hyperoxic responses and no data are available about the effects of hyperoxia in postnatal liver haematopoiesis. The aim of the study was to analyse the effects of hyperoxia in the liver tissue (hepatocytes and haemopoietic cells) and to investigate possible changes in the expression of Vascular Endothelial Growth Factor (VEGF), Matrix Metalloproteinase 9 (MMP-9), Hypoxia-Inducible Factor-1α (HIF-1α), endothelial Nitric Oxide Synthase (eNOS), and Nuclear Factor-kB (NF-kB). Experimental design of the study involved exposure of newborn rats to room air (controls), 60% O2 (moderate hyperoxia), or 95% O2 (severe hyperoxia) for the first two postnatal weeks. Immunohistochemical and Western blot analyses were performed. Severe hyperoxia increased hepatocyte apoptosis and MMP-9 expression and decreased VEGF expression. Reduced content in reticular fibers was found in moderate and severe hyperoxia. Some other changes were specifically produced in hepatocytes by moderate hyperoxia, i.e., upregulation of HIF-1α and downregulation of eNOS and NF-kB. Postnatal severe hyperoxia exposure increased liver haemopoiesis and upregulated the expression of VEGF (both moderate and severe hyperoxia) and eNOS (severe hyperoxia) in haemopoietic cells. In conclusion, our study showed different effects of hyperoxia on hepatocytes and haemopoietic cells and differential involvement of the above factors. The involvement of VEGF and eNOS in the liver haemopoietic response to hyperoxia may be hypothesized.
    Full-text · Article · Aug 2014 · PLoS ONE
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    • "The goal of ventilator treatment is to balance gas exchange while minimising trauma to the lung tissue [3]. Adjusting oxygenation and ventilator therapy is challenging, and improved strategies are needed to minimise hyperoxemia [4] and hyperventilation with hypocarbia [5,6] in preterm and full-term newborns. Appropriate oxygenation is achieved by titrating the fraction of inspired oxygen (FiO2) and the mean airway pressure (MAP). "
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    ABSTRACT: Ventilator treatment exposes newborns to both hyperoxemia and hyperventilation. It is not known how common hyperoxemia and hyperventilation are in neonatal intensive care units in Norway. The purpose of this study was to assess the quality of current care by studying deviations from the target range of charted oxygenation and ventilation parameters in newborns receiving mechanical ventilation. Single centre, retrospective chart review that focused on oxygen and ventilator treatment practices. The bedside intensive care charts of 138 newborns reflected 4978 hours of ventilator time. Arterial blood gases were charted in 1170 samples. In oxygen-supplemented newborns, high arterial pressure of oxygen (PaO2) values were observed in 87/609 (14%) samples. In extremely premature newborns only 5% of the recorded PaO2 values were high. Low arterial pressure of CO2 (PaCO2) values were recorded in 187/1170 (16%) samples, and 64 (34%) of these were < 4 kPa. Half of all low values were measured in extremely premature newborns. Tidal volumes above the target range were noted in 22% of premature and 20% of full-term newborns. There was a low prevalence of high PaO2 values in premature newborns, which increased significantly with gestational age (GA). The prevalence of low PaCO2 values was highest among extremely premature newborns and decreased with increasing GA. Further studies are needed to identify whether adherence to oxygenation and ventilation targets can be improved by clearer communication and allocation of responsibilities between nurses and physicians.
    Full-text · Article · Aug 2013 · BMC Pediatrics
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    • "Supplemental oxygen is a common, and life saving, strategy used in neonatal intensive care units [1]. However, exposure to high concentrations of oxygen causes increased oxidative stress [2-4], inflammation [5,6] and damage to lung tissues [2-7]. Persistent exposure to hyperoxia eventually results in irreversible pulmonary toxicity and death [8]. "
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    ABSTRACT: Oxygen may damage the lung directly via generation of reactive oxygen species (ROS) or indirectly via the recruitment of inflammatory cells, especially neutrophils. Overexpression of extracellular superoxide dismutase (EC-SOD) has been shown to protect the lung against hyperoxia in the newborn mouse model. The CXC-chemokine receptor antagonist (Antileukinate) successfully inhibits neutrophil influx into the lung following a variety of pulmonary insults. In this study, we tested the hypothesis that the combined strategy of overexpression of EC-SOD and inhibiting neutrophil influx would reduce the inflammatory response and oxidative stress in the lung after acute hyperoxic exposure more efficiently than either single intervention. Neonate transgenic (Tg) (with an extra copy of hEC-SOD) and wild type (WT) were exposed to acute hyperoxia (95% FiO2 for 7 days) and compared to matched room air groups. Inflammatory markers (myeloperoxidase, albumin, number of inflammatory cells), oxidative markers (8-isoprostane, ratio of reduced/oxidized glutathione), and histopathology were examined in groups exposed to room air or hyperoxia. During the exposure, some mice received a daily intraperitoneal injection of Antileukinate. Antileukinate-treated Tg mice had significantly decreased pulmonary inflammation and oxidative stress compared to Antileukinate-treated WT mice (p < 0.05) or Antileukinate-non-treated Tg mice (p < 0.05). Combined strategy of EC-SOD and neutrophil influx blockade may have a therapeutic benefit in protecting the lung against acute hyperoxic injury.
    Full-text · Article · Jul 2012 · Respiratory research
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