Timing Neonatal Hypoxic-Ischemic Encephalopathy

Abstract

Therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy initiated within six hours after birth effectively prevents neurodevelopmental impairments in some but not all infants. In part, this may be related to the timing of hypoxia before birth relative to the initiation of cooling. Metabolic acidosis at birth (suggesting acute hypoxia-ischemia) is required for treatment with hypothermia. However, placental evidence suggests that some infants also have chronic hypoxemia or poor perfusion before birth. Furthermore, although fetal distress is often noted during labor, timing the inciting event is difficult without a discrete sentinel event (such as umbilical cord prolapse). Another potential method of timing the onset of fetal hypoxia is through the evaluation of neonatal nucleated red blood cell counts. Fetal hypoxia induces production of erythropoietin and then nucleated red blood cells. These cells first appear in the blood at 24-36 hours after administration of darbepoetin in newborn infants,1Christensen R.D. Lambert D.K. Richards D.S. Estimating the nucleated red blood cell ‘emergence time’ in neonates.J Perinatol. 2014; 34: 116-119https://doi.org/10.1038/jp.2013.113Crossref PubMed Scopus (20) Google Scholar suggesting that elevated counts at birth reflect hypoxic events at least 24 hours earlier. In this volume of The Journal of Pediatrics, Bahr et al. report that infants with sentinel events during labor did not have elevated nucleated red cell counts at birth (>95% for age) and that normal counts were associated with somewhat better neurodevelopmental outcomes. Further work in this area, perhaps combined with biomarker studies and placental evaluations, may help researchers identify infants with a longer duration of fetal hypoxia who may not respond to therapeutic hypothermia alone. Research on new therapies could then be targeted to those who are most likely to benefit. Article page 12