6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Early Hypoxemia Burden is Strongly Associated with Severe Intracranial Hemorrhage in Preterm Infants

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objectives:

          The objective of this study was to define the association between the burden of severe hypoxemia (SpO 2≤70%) in the first week of life and development of severe ICH (grade III/IV) in preterm infants.

          Study Design:

          Infants born <32 weeks or weighing <1500g underwent prospective SpO 2 recording from birth through 7d. Severe hypoxemia burden was calculated as the percentage of the error-corrected recording where SpO 2≤70%. Binary logistic regression was used to model the relationship between hypoxemia burden and severe ICH.

          Results:

          A total of 163.3 million valid SpO 2 data points were collected from 645 infants with mean EGA=27.7±2.6 weeks, BW=1005±291g; 38/645 (6%) developed severe ICH. There was a greater mean hypoxemia burden for infants with severe ICH (3%) compared to those without (0.1%) and remained significant when controlling for multiple confounding factors.

          Conclusion:

          The severe hypoxemia burden in the first week of life is strongly associated with severe ICH.

          Related collections

          Most cited references31

          • Record: found
          • Abstract: found
          • Article: not found

          Vascular-specific growth factors and blood vessel formation.

          A recent explosion in newly discovered vascular growth factors has coincided with exploitation of powerful new genetic approaches for studying vascular development. An emerging rule is that all of these factors must be used in perfect harmony to form functional vessels. These new findings also demand re-evaluation of therapeutic efforts aimed at regulating blood vessel growth in ischaemia, cancer and other pathological settings.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Intraventricular hemorrhage in premature infants: mechanism of disease.

            Intraventricular hemorrhage (IVH) is a major complication of prematurity. IVH typically initiates in the germinal matrix, which is a richly vascularized collection of neuronal-glial precursor cells in the developing brain. The etiology of IVH is multifactorial and is primarily attributed to the intrinsic fragility of the germinal matrix vasculature and the disturbance in the cerebral blood flow (CBF). Although this review broadly describes the pathogenesis of IVH, the main focus is on the recent development in molecular mechanisms that elucidates the fragility of the germinal matrix vasculature. The microvasculature of the germinal matrix is frail because of an abundance of angiogenic blood vessels that exhibit paucity of pericytes, immaturity of basal lamina, and deficiency of glial fibrillary acidic protein (GFAP) in the ensheathing astrocytes endfeet. High VEGF and angiopoietin-2 levels activate a rapid angiogenesis in the germinal matrix. The elevation of these growth factors may be ascribed to a relative hypoxia of the germinal matrix perhaps resulting from high metabolic activity and oxygen consumption of the neural progenitor cells. Hence, the rapid stabilization of the angiogenic vessels and the restoration of normal CBF on the first day of life are potential strategies to prevent IVH in premature infants.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Target ranges of oxygen saturation in extremely preterm infants.

              Previous studies have suggested that the incidence of retinopathy is lower in preterm infants with exposure to reduced levels of oxygenation than in those exposed to higher levels of oxygenation. However, it is unclear what range of oxygen saturation is appropriate to minimize retinopathy without increasing adverse outcomes. We performed a randomized trial with a 2-by-2 factorial design to compare target ranges of oxygen saturation of 85 to 89% or 91 to 95% among 1316 infants who were born between 24 weeks 0 days and 27 weeks 6 days of gestation. The primary outcome was a composite of severe retinopathy of prematurity (defined as the presence of threshold retinopathy, the need for surgical ophthalmologic intervention, or the use of bevacizumab), death before discharge from the hospital, or both. All infants were also randomly assigned to continuous positive airway pressure or intubation and surfactant. The rates of severe retinopathy or death did not differ significantly between the lower-oxygen-saturation group and the higher-oxygen-saturation group (28.3% and 32.1%, respectively; relative risk with lower oxygen saturation, 0.90; 95% confidence interval [CI], 0.76 to 1.06; P=0.21). Death before discharge occurred more frequently in the lower-oxygen-saturation group (in 19.9% of infants vs. 16.2%; relative risk, 1.27; 95% CI, 1.01 to 1.60; P=0.04), whereas severe retinopathy among survivors occurred less often in this group (8.6% vs. 17.9%; relative risk, 0.52; 95% CI, 0.37 to 0.73; P<0.001). There were no significant differences in the rates of other adverse events. A lower target range of oxygenation (85 to 89%), as compared with a higher range (91 to 95%), did not significantly decrease the composite outcome of severe retinopathy or death, but it resulted in an increase in mortality and a substantial decrease in severe retinopathy among survivors. The increase in mortality is a major concern, since a lower target range of oxygen saturation is increasingly being advocated to prevent retinopathy of prematurity. (ClinicalTrials.gov number, NCT00233324.) 2010 Massachusetts Medical Society
                Bookmark

                Author and article information

                Journal
                8501884
                5061
                J Perinatol
                J Perinatol
                Journal of perinatology : official journal of the California Perinatal Association
                0743-8346
                1476-5543
                12 September 2018
                28 September 2018
                January 2019
                28 March 2019
                : 39
                : 1
                : 48-53
                Affiliations
                [1 ]Department of Pediatrics, Washington University School of Medicine, Division of Newborn Medicine, St. Louis, MO
                [2 ]Department of Medicine, University of Virginia, Charlottesville, VA
                [3 ]Department of Pediatrics, University of Virginia, Charlottesville, VA
                [4 ]Department of Pediatrics, Columbia University, New York, NY
                Author notes
                Address correspondence to: Zachary A. Vesoulis, MD, 1 Children’s Place, Box 8116, St. Louis, MO 63110, Phone: 314-454-6148, Fax: 314-454-4633, vesoulis_z@ 123456wustl.edu
                Article
                NIHMS1506375
                10.1038/s41372-018-0236-2
                6298838
                30267001
                4c0a0299-867f-4c10-b8f4-2d9c40faee00

                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Categories
                Article

                Pediatrics
                Pediatrics

                Comments

                Comment on this article