Diagnosis and treatment of neonatal jaundice

  Neonatal jaundice is a condition characterized by elevated bilirubin levels in the blood due to abnormal bilirubin metabolism in the neonatal period and appears as jaundice of the skin, mucous membranes and sclera.  Diagnosis 1. To determine whether pathological jaundice is present Neonates are prone to increased blood bilirubin and clinical jaundice due to increased bilirubin production, immature liver function, and enterohepatic circulation. Because unconjugated bilirubin concentration reaches a certain level, it can damage brain cells through the blood-brain barrier (often called nuclear jaundice), causing death or sequelae such as cerebral palsy and mental retardation. Therefore, determining whether neonatal jaundice is physiological or pathological is the first step in diagnosis.  Physiological jaundice is a gradual rise in serum bilirubin from 17 to 51 μmol/L at birth to 86 μmol/L or more 24 hours after birth, often appearing 2 to 3 days after birth, peaking at 4 to 6 days and subsiding in 7 to 10 days, lasting longer in premature infants, with no clinical symptoms other than a slight loss of appetite. In physiologic jaundice, serum bilirubin does not exceed 204 μmol/L in term infants and 255 μmol/L in preterm infants, but individual preterm infants with serum bilirubin less than 204 μmol/L can also develop bilirubin encephalopathy, at which time physiologic jaundice should be alert to prevent misdiagnosis or underdiagnosis of pathologic jaundice.  Pathological jaundice in newborns has the following characteristics: ① jaundice appears early, within 24 hours after birth; ② jaundice is heavy, golden yellow or jaundice throughout the body, palms, soles also have more obvious jaundice or serum bilirubin greater than 204-255μmol/L; ③ jaundice lasting, 2-3 weeks after birth jaundice still persists or even deepen, or reduce and then deepen; ④ accompanied by anemia or ④ with anemia or pale stool color; ⑤ with abnormal body temperature, poor appetite, vomiting and other manifestations.  2, to determine whether surgical jaundice based on medical history, symptoms of jaundice and accompanying clinical manifestations, laboratory tests and other ancillary tests to identify medical and surgical jaundice. In addition to congenital bilirubin metabolism defects, hemolytic diseases, sepsis, severe hypoxia, hypoglycemia, galactosemia, severe dehydration, alpha-antitrypsin deficiency, and drugs can cause pediatric medical jaundice. Pediatric surgical jaundice is mostly combined bilirubinemia, collectively referred to as obstructive jaundice, and can be divided into intrahepatic stasis jaundice and extrahepatic obstructive jaundice. Intrahepatic stasis jaundice is a lesion located above the intrahepatic bile ducts and can be seen in pediatric patients with viral hepatitis, intrahepatic capillary cholangitis, and cirrhosis. Extrahepatic obstructive jaundice is a mechanical obstruction below grade 1~2 bile ducts and can be seen in congenital abnormalities in the development of the biliary system and acquired obstruction of the extrahepatic bile ducts.  3. laboratory tests 4. ancillary tests (1) ultrasonography (2) hepatobiliary dynamic nuclear imaging (3) magnetic resonance hydrography (4) retrograde cholangiopancreatography (5) puncture pathological histology (6) laparoscopy with cholangiography Differential diagnosis Jaundice in the neonatal period is more common than at any other age and has a complex etiology, mainly the differentiation between congenital biliary atresia and neonatal hepatitis syndrome, because the two The clinical manifestations are similar, but the treatment is different. Biliary atresia needs to be treated with surgery as early as possible, within 60 days of age, and the postoperative bile excretion rate can be 82% to 90%. The rate of jaundice regression is 55%~66%, and the delay in surgery, the worse the surgical effect. If the time is too late, irreversible cirrhosis may occur and the opportunity for surgery is lost. Therefore, the cause of jaundice should be clarified as soon as possible and the appropriate treatment should be selected for timely treatment.  In addition to the identification of neonatal hepatitis syndrome and congenital biliary atresia, attention should also be paid to the following types of pathological jaundice, such as hemolytic jaundice, infectious jaundice and breast milk jaundice, because pathological jaundice, regardless of the cause, can cause “nuclear jaundice” in severe cases, and its prognosis is poor, in addition to neurological damage. In addition to neurological damage, severe cases can cause death.  The diagnosis and treatment of neonatal jaundice are often carried out simultaneously, and once biliary atresia is highly suspected or if medical treatment for cholestatic biliary obstruction is ineffective despite the hepatitis syndrome, surgery should be performed and treated accordingly.  The purpose of surgery is to further define the cause of biliary obstruction, eliminate the cause, reconstruct or unblock the bile duct, improve the biliary sludge state and promote liver function recovery.