Neonatal jaundice is a common clinical condition, occurring in about 50-60% of full-term newborns and up to 80% of preterm infants. This is due to the high production of bilirubin in newborns, the imperfect development of liver function, the lack of ability to transport bilirubin and the characteristics of the intestinal and hepatic circulation, manifested as a phenomenon of sclera, skin, mucous membranes, body fluids and other tissues dyed yellow visible to the naked eye during the neonatal period, divided into two kinds of physiological and pathological. Physiological jaundice generally appears 2-3 days after birth, peaks at 4-5 days, and subsides naturally in 10-14 days, and may be delayed to 3-4 weeks in premature infants. Serum bilirubin concentration does not exceed 205 μmol/L (12 mg/dl) in term infants and 256 μmol/L (15 mg/dl) in preterm infants. Pathological jaundice occurs when the bilirubin concentration reaches a certain level. Pathological jaundice appears early (24 hours after birth), jaundice is severe, progresses rapidly, and is delayed (more than 2 weeks in term infants and more than 4 weeks in preterm infants), and the jaundice recedes and recurs or worsens progressively. Clinically, a total bilirubin >220.6 μmol/L (12.9 mg/dl) in term infants and >256.5 μmol/L (15 mg/dl) in preterm infants are used as diagnostic criteria for neonatal hyperbilirubinemia. Bilirubin encephalopathy may occur when total bilirubin is >342 μmol/L (20 mg/dl). However, there is no one-size-fits-all criterion for physiological jaundice and pathological jaundice, and a comprehensive assessment is needed to determine the diagnosis in relation to the gestational age at birth, birth weight, presence of high-risk factors, age at appearance of jaundice, speed of jaundice aggravation, and other etiologies, and then to give treatment recommendations.