Improvements in the detection of fetal and neonatal brain injuries, advances in our understanding of the pathophysiology, cellular and molecular bases of encephalopathy, and new treatment options have all combined to produce significant changes in the management of neonatal brain disorders in the past few years. This new edition of Fetal and Neonatal Brain Injury brings the reader fully up to date with all advances in clinical management and outcome assessment. Updated material includes inflammation focusing in particular on chorioamnionitis and fetal brain injury; genetic brain injury; and expanded sections on cholestasis, diabetes, and thyroid disease. An updated, highly illustrated chapter on structural and functional imaging of the fetal and neonatal brain is also included. An outstanding international team of highly experienced neonatologists and maternal-fetal medicine clinicians have produced a practical, authoritative clinical text that gives clear management advice to all clinicians involved in the treatment of these patients.

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 benefit form 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.