Neonatal Hyperbilirubinemia in Preterm Neonates, An Issue of Clinics in Perinatology, 1st Edition
Authors :
David K. Stevenson & Vinod K. Bhutani
Preterm neonates remain at increased risk for adverse bilirubin-related outcomes, including acute bilirubin encephalopathy relative to term infants. Yet, most vulnerable neonates are likely to benefit from the potent anti-oxidant properties of biliru ...view more
Preterm neonates remain at increased risk for adverse bilirubin-related outcomes, including acute bilirubin encephalopathy relative to term infants. Yet, most vulnerable neonates are likely to benefit from the potent anti-oxidant properties of bilirubin. Evidence-based guidelines for the management of hyperbilirubinemia in preterm infants, however, are lacking. High concentrations of unconjugated bilirubin can cause permanent neurologic damage in infants, evident through magnetic resonance imaging of chronic bilirubin encephalopathy or kernicterus. There is a growing concern that exposures to even moderate concentrations of bilirubin may lead to subtle but permanent neurodevelopmental impairment referred to as bilirubin-induced neurologic dysfunction. Our current use of phototherapy to decrease bilirubin loads and its potential photo-oxidant properties is a biological conundrum that has been questioned in the use of phototherapy for very low birth weight neonates. In this issue of Clinics in Perinatology, we provide updates on the current understanding of the biology, mechanisms of increasing bilirubin load due to hemolysis, decreased bilirubin binding capacity and glucose-6-phosphate dehydrogenase deficiency, as well as clinical strategies to operationalize the thresholds for hyperbilirubinemia interventions in preterm infants.
Preterm neonates remain at increased risk for adverse bilirubin-related outcomes, including acute bilirubin encephalopathy relative to term infants. Yet, most vulnerable neonates are likely to benefit from the potent anti-oxidant properties of bilirubin. Evidence-based guidelines for the management of hyperbilirubinemia in preterm infants, however, are lacking. High concentrations of unconjugated bilirubin can cause permanent neurologic damage in infants, evident through magnetic resonance imaging of chronic bilirubin encephalopathy or kernicterus. There is a growing concern that exposures to even moderate concentrations of bilirubin may lead to subtle but permanent neurodevelopmental impairment referred to as bilirubin-induced neurologic dysfunction. Our current use of phototherapy to decrease bilirubin loads and its potential photo-oxidant properties is a biological conundrum that has been questioned in the use of phototherapy for very low birth weight neonates. In this issue of Clinics in Perinatology, we provide updates on the current understanding of the biology, mechanisms of increasing bilirubin load due to hemolysis, decreased bilirubin binding capacity and glucose-6-phosphate dehydrogenase deficiency, as well as clinical strategies to operationalize the thresholds for hyperbilirubinemia interventions in preterm infants.
Author Information
By David K. Stevenson, MD, Harold K. Faber Professor of Pediatrics, Senior Associate Dean for Maternal & Child Health, Co-Director, Maternal and Child Health Research Institute, Stanford University School of Medicine and Vinod K. Bhutani, MD, FAAP, Lucile Salter Packard Children's Hospital, Palo Alto, CA
https://www.us.elsevierhealth.com/neonatal-hyperbilirubinemia-in-preterm-neonates-an-issue-of-clinics-in-perinatology-9780323446280.html2274Neonatal Hyperbilirubinemia in Preterm Neonates, An Issue of Clinics in Perinatologyhttps://www.us.elsevierhealth.com/media/catalog/product/9/7/9780323446280.jpg70.84108.99USDInStock/Medicine/Obstetrics/Gynecology/Clinics/Clinics3834388725525504113841826925145120<p>Preterm neonates remain at increased risk for adverse bilirubin-related outcomes, including acute bilirubin encephalopathy relative to term infants. Yet, most vulnerable neonates are likely to benefit from the potent anti-oxidant properties of bilirubin. Evidence-based guidelines for the management of hyperbilirubinemia in preterm infants, however, are lacking. High concentrations of unconjugated bilirubin can cause permanent neurologic damage in infants, evident through magnetic resonance imaging of chronic bilirubin encephalopathy or kernicterus. There is a growing concern that exposures to even moderate concentrations of bilirubin may lead to subtle but permanent neurodevelopmental impairment referred to as bilirubin-induced neurologic dysfunction. Our current use of phototherapy to decrease bilirubin loads and its potential photo-oxidant properties is a biological conundrum that has been questioned in the use of phototherapy for very low birth weight neonates. In this issue of Clinics in Perinatology, we provide updates on the current understanding of the biology, mechanisms of increasing bilirubin load due to hemolysis, decreased bilirubin binding capacity and glucose-6-phosphate dehydrogenase deficiency, as well as clinical strategies to operationalize the thresholds for hyperbilirubinemia interventions in preterm infants.</p> <p>Preterm neonates remain at increased risk for adverse bilirubin-related outcomes, including acute bilirubin encephalopathy relative to term infants. Yet, most vulnerable neonates are likely to benefit from the potent anti-oxidant properties of bilirubin. Evidence-based guidelines for the management of hyperbilirubinemia in preterm infants, however, are lacking. High concentrations of unconjugated bilirubin can cause permanent neurologic damage in infants, evident through magnetic resonance imaging of chronic bilirubin encephalopathy or kernicterus. There is a growing concern that exposures to even moderate concentrations of bilirubin may lead to subtle but permanent neurodevelopmental impairment referred to as bilirubin-induced neurologic dysfunction. Our current use of phototherapy to decrease bilirubin loads and its potential photo-oxidant properties is a biological conundrum that has been questioned in the use of phototherapy for very low birth weight neonates. In this issue of Clinics in Perinatology, we provide updates on the current understanding of the biology, mechanisms of increasing bilirubin load due to hemolysis, decreased bilirubin binding capacity and glucose-6-phosphate dehydrogenase deficiency, as well as clinical strategies to operationalize the thresholds for hyperbilirubinemia interventions in preterm infants.</p>00add-to-cart97803234462802016ProfessionalBy David K. Stevenson, MD and Vinod K. Bhutani, MD, FAAP20161BookOtherElsevier0Jun 9, 2016IN STOCK - This may take up to 5 business days to shipBy <STRONG>David K. Stevenson</STRONG>, MD, Harold K. Faber Professor of Pediatrics, Senior Associate Dean for Maternal & Child Health, Co-Director, Maternal and Child Health Research Institute, Stanford University School of Medicine and <STRONG>Vinod K. Bhutani</STRONG>, MD, FAAP, Lucile Salter Packard Children's Hospital, Palo Alto, CAClinicsClinicsThe Clinics: Internal MedicineNoNoNoNoPlease SelectPlease SelectPlease Select
