Umbilical Artery Blood Gas Parameters in Neonates With Early-Onset Seizures Who Die

Abstract

Hypoxic–ischemic encephalopathy is diagnosed when newborn infants have certain neurologic abnormalities, including early-onset seizures, within 24–48 hours of admission to neonatal intensive care. The American College of Obstetricians and Gynecologists defines hypoxia severe enough to cause hypoxic–ischemic encephalopathy as a group of findings including a pH below 7.0; an Apgar score of 0–3 for longer than 5 minutes; neurologic sequelae; and cardiovascular, gastrointestinal, hematologic, pulmonary, or renal dysfunction. Early-onset seizures are the clearest indicator of moderate to severe disease with hypoxic–ischemic encephalopathy. Infants with this disorder are also at increased risk of cerebral palsy and neonatal death. This study sought to relate umbilical artery blood gas parameters to mortality in 47 infants at 32 or more weeks gestation who were admitted with early-onset seizures secondary to hypoxic–ischemic encephalopathy. Fourteen of 47 newborn infants admitted to the study died of complications related to hypoxic–ischemic encephalopathy. Maternal demographic factors were comparable regardless of whether the infant died or survived. Active resuscitation was attempted in all instances. There were no significant differences between infants who died and those who survived with respect to umbilical artery blood values of pH, base deficit, PCO2, or oxygen saturation. Levels of PO2 were significantly higher in neonates who died than in survivors (18.4 vs. 12.3). Neither umbilical artery blood pH nor base deficit predicted neonatal deaths in the present study of infants having hypoxic–ischemic encephalopathy and early-onset seizures. A high PO2 in newborn infants who subsequently die may reflect an impaired inability to extract oxygen from the blood. The question of whether patterns of change in PCO2 predict the development of neonatal encephalopathy awaits further investigation.