There are more available experimental methods, but all have poor specificity. In biliary atresia, total serum bilirubin is increased, and the proportion of one-minute bilirubin is correspondingly increased. The abnormally high value of alkaline phosphatase has a reference value for diagnosis. Υ-glutamyltransferase The peak value is higher than 300 IU/L, which is persistently high or rapidly increasing. 5′ nucleotidase is higher when the bile duct hyperplasia is significant, and the measured value is >25 IU/L. The method of erythrocyte peroxide hemolysis test is more complicated, and it is positive if the hemolysis is above 80%. The peak value of methemoglobin is less than 40 μg/ml, and the results of other routine liver function tests have no discriminatory significance. For the onset of jaundice, the color change of stool, and the physical examination of the abdomen, tracing observations should be made for a comprehensive analysis. At present, the following tests are considered to have some diagnostic value. (a) Dynamic observation of serum bilirubin: weekly measurement of serum bilirubin, if the curve of bilirubin amount tends to decline with the course of the disease, it may be hepatitis; if it continues to rise, it suggests biliary atresia. However, when heavy hepatitis is accompanied by extrahepatic biliary obstruction, it may also show a continuous rise, and it is difficult to identify it. (B) Ultrasonography: If no gallbladder is seen or if a small gallbladder (less than 1.5 cm) is seen, biliary atresia is suspected. If a normal gallbladder is seen to be present, hepatitis is supported. If the distribution pattern of intrahepatic bile ducts can be seen, it will be more helpful for diagnosis. (iii) 99mTc-diethyl iminodiacetic acid (DIDA) excretion test: In recent years, it has replaced the 131 iodine-labeled rosacea excretion test and has a high hepatocyte extraction rate (48% to 56%), which is better than other items. It can diagnose partial obstruction of the biliary tract due to structural abnormalities. If a common bile duct cyst or extrahepatic bile duct stenosis occurs with complete obstruction, the scan does not show intestinal visualization and can be used as a differentiator for severe intrahepatic biliary depression. In the early stages of biliary atresia, the hepatocytes function well and the liver image is visible in 5 minutes, but no biliary tract image is seen later, even after 24 hours, and no intestinal image is seen. In neonatal hepatitis, the extrahepatic bile ducts are open and the intestinal tract is visualized, although the hepatocytes are not functioning well. (iv) Quantification of lipoprotein-X (Lp-x): Lipoprotein-X is a low-density lipoprotein that is elevated in cases of biliary obstruction. According to the study, all cases of biliary atresia are elevated and are positive at a very young age, while neonatal hepatitis cases are negative in the early stages but can turn positive with increasing age. If the birth is more than 4 weeks and Lp-X is negative, biliary atresia can be excluded; if >500mg/dl, biliary atresia is more likely. If the level decreases, the diagnosis of neonatal hepatitis syndrome is supported; if it continues to rise, biliary atresia is possible. (E) quantitative determination of bile acids: recently applied to the blood paper serum total bile acids quantitative method, total serum bile acids in biliary atresia is 107-294μmol/L, generally considered up to 100μmol/L are depressed bile, the same age without jaundice control group is only 5-33μmol/L, the average is 18μmol/L, so it has diagnostic value. Urinary bile acids are also a means of early screening. The mean urinary total bile acids in biliary atresia was 19.93±7.53μmol/L, compared with 1.60±0.16μmol/L in the control group, which was 10 times greater than that of normal children. (vi) Cholangiography: ERCP has been applied for early differential diagnosis. The following conditions of biliary atresia are found on imaging: (i) only the pancreatic duct is visualized; (ii) sometimes abnormal pancreaticobiliary duct co-flow can be found, and both the pancreatic duct and bile duct can be visualized, but the intrahepatic bile duct is not visualized, suggesting intrahepatic type atresia. Neonatal hepatitis syndrome has the following signs: (1) the pancreaticobiliary ducts are normal; (2) the common bile ducts are visualized, but are thin. (g) Hepatic puncture pathological histological examination: liver puncture biopsy, or percutaneous hepatic puncture imaging and biopsy are generally advocated. Neonatal hepatitis is characterized by irregular arrangement of lobular structures, hepatocyte necrosis, giant cellular degeneration and portal inflammation. The main manifestations of biliary atresia are marked bile duct hyperplasia and bile embolism, and periportal fibrosis, although multinucleated giant cells may be seen in some specimens. Therefore, liver biopsy can sometimes be diagnostically difficult or even wrong, and in 10-15% of cases the correct diagnosis cannot be made on the basis of this. In conclusion, once biliary atresia is highly suspected in the first month of life, a variety of differential diagnostic methods should be performed, such as clinical, laboratory, ultrasound, radiological, and tissue biopsy, and surgical exploration should also be considered. In cases where the duration of the disease is close to 2 months and the diagnosis is still unknown, a right upper abdominal incision should be made to obtain a liver tissue specimen and cholangiogram with minimal manipulation. If the gallbladder is found, normal bile is obtained by puncture, suggesting that the proximal biliary system is not occluded, and intraoperative imaging is performed to determine the distal biliary system. If the extrahepatic bile ducts are not occluded, an excisional biopsy or puncture biopsy is performed from both liver lobes to facilitate diagnosis. In case of small and atrophied gallbladder with white bile, cholangiography should still be attempted, as deflated gallbladder can be seen in neonatal hepatitis with severe intrahepatic bile accumulation or intrahepatic bile duct deficiency. If the angiogram shows small and dysplastic extrahepatic bile ducts, but they are patent, the procedure will end with a biopsy. If the gallbladder is atretic or absent, the tissue of the hilar region is dissected to perform a hilar-enteric anastomosis. In typical cases of biliary atresia, the infant is born at term and is often regarded as normal by parents and physicians at 1 to 2 weeks after birth, with most having no abnormalities and normal fecal color. The stool becomes brownish-yellow, yellowish, beige, and later becomes a bile-free clay-like grayish white. However, in the more advanced stages of the disease, a slight yellowish color may occasionally appear, due to the increased concentration of bile pigments in the blood and other organs and a small amount of bile pigments entering the intestinal lumen via the intestinal mucosa and mixing into the stool. The urine is darker and stains the diaper yellow. After the appearance of jaundice, it usually does not subside and becomes increasingly deep, the skin becomes golden yellow or even brown, there may be scratch marks due to scratching, sometimes lipomatous fibroids may appear, but it is not common. Individual cases may develop pestle-like fingers or be accompanied by cyanosis. The liver is enlarged and hard in texture. The spleen is rarely palpable in the early stages, and if an enlarged spleen is palpable in the first few weeks, it may be an intrahepatic cause of portal hypertension that develops as the disease progresses. In the early stages of the disease, the infant is still in good general condition, but has varying degrees of malnutrition and is underweight for length and weight. Often the mother describes the infant as appearing excited and restless, a condition that may be associated with increased serum bile acids. Various fat-soluble vitamin deficiencies may occur later in the course of the disease, and vitamin D deficiency may be associated with rickets crossties and broad epiphyses. Due to altered hemodynamic status, partial arteriovenous short-circuiting and decreased peripheral vascular resistance, a high-volume heart murmur may be heard in the precordial region and lung fields.