Hyperbilirubinemia In Late Preterm Infants Research Articles

Improving Evaluation and Treatment of Hyperbilirubinemia in Late Preterm Infants.

Late preterm (LPT) infants are at an increased risk for hyperbilirubinemia. Accurate identification and early treatment are needed for optimal health outcomes. In a newborn nursery at an academic medical center, bilirubin levels were drawn at 24 hours of life, per protocol. These infants were rarely treated at this time. Rather, predischarge bilirubin levels (at about 48 hours of life) would indicate treatment, often leading to increased length of hospital stay. The practice change evaluation was conducted using retrospective medical record review. Practice change to test serum bilirubin levels at 36 hours of life rather than 24 hours of life. Compliance with the practice change was achieved (P < .05). More LPT infants were identified and treated for hyperbilirubinemia without an increase in length of stay. Readmissions for hyperbilirubinemia and blood draw rates also declined. Although more LPT infants were identified and treated for hyperbilirubinemia, there is room for improvement, and increased adherence to the policy might yield an even greater impact on quality and safety of care surrounding bilirubin management.

Does the Use of Antenatal Corticosteroids Decrease Levels of Neonatal Hyperbilirubinemia in Preterm Infants? [15K

INTRODUCTION: The use of prenatal corticosteroids for pregnant women between 34-36 6/7 weeks of pregnancy is recommended to reducing the morbidity of late preterm infants. METHODS: This is a secondary analysis of a randomized clinical trial conducted to determine the effectiveness of corticosteroids in reducing respiratory disorders in infants born at 34-36 weeks' gestation Trial registration Clinical Trials NCT00675246. This study was approved by IRB and all participants signed an informed consent term. RESULTS: Of 245 preterm infants, the number of newborns with gestational age 34, 35 and 36 was 30 (12.2%), 110 (45.1%), and 105 (42.7%), respectively. Jaundice occurred in 150 (62.5%) newborns and 70 among them required phototherapy during hospitalization. Late preterm infants exposed to corticosteroids started treatment with lifetime of 61.2± 33.6 h vs. 48.3± 25.3 h (p = 0.03) with similar levels of bilirubin (12.1± 3.2 mg/dL vs. 12.8± 3.7 mg/dL, p = 0.38) when compared to the control group. They required less treatment compared to the placebo group (n = 27 vs. n = 42, p = 0.025), and spent less days on phototherapy (1.7± 1.7 vs. 2.6± 2.2, p = 0.05). CONCLUSION: Late preterm infants exposed to prenatal corticosteroids had less need for phototherapy and shorter treatment. Also, they developed elevated level of bilirubin later. This result suggests that prenatal corticosteroids decrease the levels of hyperbilirubinemia in late preterm infants.

Risk of BIND and kernicterus in late preterm

Severe hyperbilirubinemia can induce devastating and permanent neurodevelopmental handicaps in infants. The occurrence of hyperbilirubinemia is higher in late preterm than in term infants, ranging from 8 to 40% of the formers according to different definitions of hyperbilirubinemia. The mechanisms by which this occurs is not completely understood, however an increased bilirubin load on hepatocyte, as result of decreased erythrocyte survival and increased erythrocyte volume, increased enterohepatic circulation of bilirubin, decreased hepatic uptake of bilirubin from plasma, defective bilirubin conjugation, and diminished serum bilirubin binding capacity play a relevant role. Hyperbilirubinemia in late preterm infants is not only more prevalent than in term neonates, but also it occurs later and is more severe and protracted. In fact, Maisels et al. (Pediatrics 2006;117:1169) demonstrated that at 72 hours of life the value of 50° percentile of trans-cutaneous bilirubin (TcB) is 9 mg/dl in 35-37 wks infants, while is 40 wks infants. Late preterm infants are at higher risk of bilirubin induced neurological dysfunction (BIND) and kernicterus than term infants. The mechanisms that potentially could explain the high susceptibility of central nervous system to bilirubin-induced damage in late preterm neonates have not been well defined. However, some of the factors that can potentially contribute are the diminished serum bilirubin binding capacity due to the lower serum albumin levels, an enhanced permeability of the blood–brain barrier to unconjugated bilirubin influx, and an immaturity of neuronal protective mechanisms. This is probably the reason why late preterm neonates are at an increased risk to develop acute bilirubin encephalopathy and or kernicterus as demonstrated in the USA pilot kernicterus registry (Semin Perinatol 2006;30:89) in which this category of infants is over-represented compared to term neonates. Thus, clinicians need to be more concerned and conscientious to identify late preterm’s risk for severe hyperbilirubinemia in view of their increased susceptibility to BIND. This can allow of planning a prevention program including nursing and parental education, screening for jaundice in the nursery, the provision of lactation support, timely post discharge follow-up, and appropriate treatment when clinically indicated.