After the birth of a child due to the appearance of hyperbilirubinemia as an increased concentration of serum bilirubin, it is most important to distinguish whether it is physiological or pathological hyperbilirubinemia. The presence of hyperbilirubinemia is revealed by the appearance of a yellowish discoloration in a child that first affects the sclera and then spreads through the body towards the legs. In order to establish the type and treatment required, the most important parameter used by neonatologists is the time of onset of jaundice. Jaundice that occurs in the first 24 hours or lasts more than a week in a premature or two weeks in a preterm infant should be closely monitored and treated to prevent the development of kernicterus after unconjugated toxic bilirubin enters the basal ganglia and brainstem. Such hyperbilirubinemia is called pathological. Pathological hyperbilirubinemia can be conjugated or unconjugated. Conjugated (direct) hyperbilirubinemias, unlike unconjugated ones, are always pathological, and their cause is hepatocyte damage or various bile duct obstructions. Unconjugated hyperbilirubinemias are the cause of many syndromes such as Gilbert's syndrome. Kernicterus as the worst outcome that can result from pathological jaundice is rare and unpredictable, and leads to many neurodevelopmental difficulties in surviving infants. On the other hand, physiological jaundice as a benign transient occurs after 72 hours of life of the newborn and disappears by the end of the week. In addition to these types of hyperbilirubinemia, there is another characteristic type of jaundice that occurs after childbirth and is called lactational jaundice. It is divided into early and late, and the core of its occurrence is considered to be the lack of the presence of the enzyme glucuronidase and pregnan-3α, 20β-diol and non-esterified fatty acids in breast milk. The diagnosis of hyperbilirubinemia includes the TSB test as the gold standard and the TcB test as a simpler, faster, and noninvasive method using a transcutaneous biliruinometer device. High TSB levels should be reduced and bilirubin neurotoxicity prevented by standard treatments including phototherapy and exanguinotransfusion and concomitant pharmacological support with phenobarbitol. The role of the nurse in hyperbilirubinemia extends from laboratory tests through maternal education to child care and nursing in bilirubin lowering procedures. Its role in planning and implementing health care through nursing diagnoses and interventions is also crucial. Conclusion: A form of hyperbilirubinemia in infants needs to be recognized in order to initiate timely treatment and avoid consequences such as kernicterus. In addition to neonatologists, nurses are also involved in this process.