Abstract

NEONATAL JAUNDICE: UNRAVELING THE MULTIFACTORIAL CAUSES AND PREGNANCY-RELATED RISKS FOR OPTIMAL NEWBORN CARE

Dr. Shaik Parveen*, Shaistha Saba, Mariyam Fatima and Tehseena Begum

ABSTRACT

Neonatal jaundice is a common condition in newborns, primarily resulting from elevated bilirubin levels due to increased production, impaired conjugation, or defective excretion. This review comprehensively explores the underlying causes of neonatal jaundice, categorized into hemolytic, hepatic, obstructive, drug-induced, and miscellaneous factors. Hemolytic causes, including Rh and ABO incompatibility and genetic RBC disorders (e.g., G6PD deficiency, hereditary spherocytosis, pyruvate kinase deficiency), contribute to excessive bilirubin production due to increased RBC breakdown. Hepatic causes, such as Crigler-Najjar and Gilbert syndromes, result from defective UDP-glucuronosyltransferase (UGT1A1) enzyme activity, leading to impaired bilirubin conjugation. Additionally, neonatal hepatitis (viral and metabolic causes) can further compromise bilirubin metabolism. Obstructive causes, including biliary atresia, choledochal cysts, and Alagille syndrome, interfere with bilirubin excretion, leading to direct hyperbilirubinemia. Drug-induced jaundice results from medications like sulfonamides and ceftriaxone, which displace bilirubin from albumin, increasing the risk of kernicterus. Overuse of oxytocin during labor and chloramphenicol toxicity can further impact bilirubin metabolism. Miscellaneous causes include prematurity, polycythemia, hypothyroidism, birth asphyxia, intrauterine growth restriction (IUGR), and breastfeeding-related jaundice. Preterm neonates are particularly vulnerable due to immature hepatic enzyme systems, whereas conditions like breast milk jaundice involve enterohepatic bilirubin recirculation.

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