Most babies have jaundice between 2 and 14 days after birth, which is known medically as hyperbilirubinemia. Jaundice is not a disease in itself, but like “fever” or “cough”, it is a symptom that can be caused by many things. Due to the physiological characteristics of newborns, this symptom is sometimes “physiological”, but if “pathological” jaundice is not correctly determined and detected in a timely manner, treatment can be delayed and may cause permanent and serious damage to the baby, even resulting in disability or death. To distinguish between “physiological” and “pathological” jaundice, we must first understand the mechanism by which neonatal jaundice occurs. In the fetus, due to the metabolic needs of the mother, the number of red blood cells transporting oxygen and the content of hemoglobin in the blood are higher, and after birth, with independent respiration, the excess red blood cells are destroyed and decomposed in the body, producing more bilirubin; in the newborn, due to the immature development of organs, the metabolic capacity of bilirubin is lower, and the metabolic capacity of premature infants is even worse; the concentration of bilirubin in the blood rises and seeps into the skin, producing Jaundice is visible to the naked eye. In normal newborns, jaundice appears 2-3 days after birth and basically subsides within 14 days, mainly on the face and trunk, but if jaundice appears on the extremities, hands and feet, it is often pathological. Simply put, jaundice that appears too early, is too severe, takes too long to subside, or reappears after the jaundice has subsided; especially when accompanied by lighter colored stools, excitement, depression, and refusal of milk, may be pathological jaundice. Physiological jaundice does not cause significant damage to the baby. When pathological jaundice occurs, in addition to the effects of the original cause of the jaundice on the child, excessive destruction of red blood cells can cause anemia in the child, affecting future growth and development, and can also affect the vision of premature infants; severe jaundice can cause nuclear jaundice, or bilirubin encephalopathy, which can be fatal or leave serious sequelae, and is particularly likely to occur in underweight premature infants. It is worth mentioning that the occurrence of bilirubin encephalopathy cannot be completely predicted by the level of serum bilirubin concentration, and many comprehensive factors can reduce the function of the blood-brain barrier, making it easy for bilirubin to enter the brain and cause brain damage. These factors include gestational age deficiency, hypoxia, asphyxia, infectious meningitis, acidosis and hypoproteinemia, drugs, starvation, and hypoglycemia. Pathological jaundice has different manifestations depending on the primary cause. Maternal-infant blood group incompatibility is the most common cause of hemolytic jaundice, and premarital physical examination, pregnancy screening and appropriate treatment can reduce the impact on the newborn. Obstruction of the hepatobiliary tract in newborns (various infections, dysplasia, stones, compression, etc.) and genetic metabolic disorders (galactosemia, glycogen accumulation disease, etc.) can cause severe obstructive jaundice. In addition, there is another type of jaundice known as breast milk jaundice, the exact pathogenesis of which is not known and requires the exclusion of other diseases before a diagnosis can be made. In the treatment of pathological jaundice, phototherapy is the preferred intervention, using special wavelengths of blue light to irradiate the skin so that the bilirubin in the skin is broken down and excreted through the intestine or in the urine, reducing the concentration of bilirubin in the blood; there are basically no complications with phototherapy, and only mild, transient side effects, such as fever, diarrhea, rash, riboflavin deficiency, and low blood calcium, etc., which can be quickly resolved with appropriate fluid increases and calcium supplements. The side effects will disappear soon. In addition to phototherapy, pharmacological treatment can be used, mainly to remove the primary disease and promote bilirubin excretion, such as antibiotics, antivirals, liver enzyme inducers, etc. Albumin, plasma and gammaglobulin can also be used for treatment; for severe jaundice, blood exchange is the most effective treatment. In addition to this, treatment with anti-infection, correction of acidosis and improvement of hypoxia are also necessary to prevent bilirubin encephalopathy. Interventions for breastfeeding jaundice should be treated differently according to different situations. Early-onset breastfeeding jaundice should be treated by encouraging frequent breastfeeding, more than 10 times a day, avoiding the addition of sugar water, monitoring changes in bilirubin concentration, and, if necessary, phototherapy. Children with late-onset breast-fed jaundice do not need to stop breastfeeding if the bilirubin concentration in the blood is not too high, but if it exceeds 15 mg/dL, breastfeeding can be suspended for 3 days, or phototherapy can be added. In conclusion, it is important to have your baby examined by an experienced pediatrician in a timely manner when jaundice occurs to clarify the diagnosis and provide appropriate treatment, without excessive therapeutic interventions or delays that may result in serious consequences.