Jaundice is a clinical symptom caused by abnormal bilirubin metabolism, retention of bilirubin in the body, increased serum bilirubin and staining of the sclera, skin, mucous membranes and other tissues yellow. In normal children, total serum bilirubin ranges from 3.4 to 17 umol/L. Over 34 umol/L (2.0 mg/dl), overt jaundice can occur, and at 17 to 32 umol/L (1 to 1.9 mg/dl), there is hyperbilirubinemia but no jaundice, called occult jaundice. Unconjugated bilirubin (indirect bilirubin) accounts for about 80%, while conjugated bilirubin (direct bilirubin) is about 20%. Jaundice must be distinguished from yellowing caused by consumption of excessive carotenoid-containing food, which has no yellowing of the sclera. Newborns can have physiological jaundice: 1, the appearance of time is mostly 2-5 days after birth; 2, the time of remission in full-term infants for 7-10 days after birth, premature infants can be as late as 3-4 weeks; 3, serum bilirubin full-term infants generally do not exceed 205.2umol/L (12mg/dl), premature infants do not exceed 256.5umol/L (15mg/dl) 4. no other symptoms and normal liver function. Pathological jaundice is actively searched for etiology, common causes: 1, excessive bilirubin production various congenital or acquired (acquired) hemolytic diseases, etc. 2, the liver uptake, transport bilirubin dysfunction caused by jaundice such as Gilbert syndrome, the disease may be related to the partial lack of hepatocyte BGT and congenital lack of Y , Z protein. Biliary stasis: (1) Various causes of hepatic inflammation, degeneration and necrosis, so that the uptake, binding and excretion of bilirubin are impaired, and often the excretion is more obvious, so it often shows biphasic increase of unconjugated bilirubin and conjugated bilirubin, and the increase of conjugated bilirubin is the main. Bilirubin can be detected in the urine, fecal bilirubin can be normal or decreased, and urinary urobilinogen can be normal or increased. Hepatitis is one of the most common causes of pediatric hepatocellular jaundice and includes viral hepatitis A, B, C, and D, cytomegalovirus, rubella virus, herpes simplex virus, toxoplasmosis, EBV, coxsackievirus, and bacterial infections. (2) congenital non-hemolytic jaundice including Dubin_-Johnson syndrome type I and Rotor syndrome type II, two familial genetic disorders in which selective excretion of organic anions by hepatocytes is impaired, manifested by increased conjugated bilirubin; (3) intrahepatic cholestatic jaundice seen in infantile hepatitis syndrome, biliary hepatitis, cholestatic (3) intrahepatic biliary jaundice is seen in infantile hepatitis syndrome, biliary hepatitis, biliary cirrhosis, certain congenital metabolic diseases such as hepatic glycogen accumulation disease, galactosemia, α1 antitrypsin deficiency, hepatomegaly, and drug intoxication. The main manifestation of cholestatic hepatitis is intrahepatic biliary stasis, which is characterized by “three separations”: ① separation of jaundice from gastrointestinal symptoms; ② separation of bile enzymes: jaundice is heavy, but ALT does not rise much, or ALT decreases with the increase of jaundice; ③ separation of jaundice from prothrombin activity. 4, extrahepatic obstruction are: congenital biliary atresia, Allage syndrome, gallstones, bile duct stenosis, common bile duct cyst, tumor compression and obstruction, post-surgical bile duct stenosis, etc.