Abstract
BackgroundThe recognition, follow-up, and early treatment of neonatal jaundice has become more difficult, since the earlier discharge of newborns from hospitals has become common practice. Since intrapartum hypoxic stress has been pointed as predisposing factor for the occurrence of hyperbilirubinemia risk, we tested the association with the cord blood acid-base index tests.MethodsA cohort of healthy term and near-term newborns underwent umbilical cord hemogasanalysis at birth and capillary heel total serum bilirubin (TSB) pre-discharge, scheduled at 36 h of life, to define the risk of significant hyperbilirubinemia, defined as >9 mg/dL TSB level, ≥ 75th percentile on nomogram of Bhutani et al.ResultsIt was found that among 537 studied neonates, 133 (24.8%) had pre-discharge TSB levels of >9 mg/dL. When the cord blood gas analysis index tests were compared, their acidemia levels were significantly higher than those of neonates with normal TSB levels: HCO3− (20.71 ± 2.37 vs. 21.29 ± 2.25 mEq/L, p < 0.010), base deficit (−3.52 ± 3.188 vs. -2.68 ± 3.266 mEq/L, p < 0.010), and lactacidemia (3.84 ± 1.864 vs. 3.39 ± 1.737 mEq/L, p < 0.012), respectively. However, logistic regression analysis showed that base deficit was the strongest index of the pre-discharge hyperbilirubinemia risk (OR, 95% CI 0.593; 0.411–0.856), and the hyperbilirubinemia risk increased by 40% with the decrease of 1 mEq/L of base deficit.ConclusionsUmbilical cord blood acidemia and lactacidemia are significant indexes of adaptive mechanisms at birth. The base deficit provides the strongest association with future development of high bilirubin on an hour specific bilirubin nomogram generating risk stratification score in term and near-term neonates.
Highlights
The recognition, follow-up, and early treatment of neonatal jaundice has become more difficult, since the earlier discharge of newborns from hospitals has become common practice
Perinatal asphyxia, as well as acidosis have been pointed as predisposing risk factors for the occurrence of significant unconjugated hyperbilirubinemia and the need of phototherapy and, by itself, can abide the risk of brain damage [11,12,13,14], In accordance with the Literature, in many cases hypoxemia and acidosis seem to be well tolerated by newborns [15], a more pronounced hypoxic insult can bear the risk of cerebral damage and/or affect the bilirubin/albumin ratio for binding and the ability of properly process bilirubin to the direct form, increasing the rate of occurrence of unconjugated bilirubin encephalopathy [16]
A total of 544 newborns were initially enrolled in the study, but 7 of these were excluded during the study because of various diagnoses, such as duodenal atresia (1 neonate), direct hyperbilirubinemia (1 neonate), and infection or sepsis (2 neonates), or because some (3 neonates) of the parents did not want to continue participating in the study refusing metabolic screenings
Summary
The recognition, follow-up, and early treatment of neonatal jaundice has become more difficult, since the earlier discharge of newborns from hospitals has become common practice. To reduce bilirubin induced neurological dysfunction incidence, the American Academy of Pediatrics recommended that all newborn infants be assessed before discharge for the risk of developing significant neonatal hyperbilirubinemia [6]. These Guidelines suggest two risk-assessment options, used individually or in combination: pre-discharge measurement of the bilirubin level and assessment of clinical maternal, infant, and delivery risk factors known to be associated with neonatal hyperbilirubinemia [7,8,9]. The accuracy of clinical risk factor assessment has been attenuated by omission of test useful to measure important clinical predictors and/or lack of hour-specific bilirubin nomogram to calculate an infant’s bilirubin percentile with respect to age in hours, to support the pre-discharge hyperbilirubinemia “risk zone” [10]
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