Physiological neonatal jaundice

Outlined is not a physiological jaundice (physiologic jaundice) is 24 newborns when the serum bilirubin from the birth of the 17-51μmol / L (1 ~ 3mg/dl) gradually increased to 86 μ mol / L (5mg/dl) or above, clinical jaundice there without other symptoms, 1 ~ 2 weeks dissipated. Physiological jaundice of serum bilirubin among full-term infants not more than 204 μmol / L (dl). Premature infants not more than 255 μmol / L (15mg/dl). However, individual serum bilirubin premature infants less than 204 μmol / L (dl) may also occur bilirubin encephalopathy , the physiological jaundice due vigilance against the pathologic jaundice misdiagnosed or missed. Cause pathogenesis gestational age of 12 weeks and amniotic fluid have bilirubin. This is the fetal trachea and bronchial tree secretion of the amniotic fluid of unconjugated bilirubin. Fetal red blood cells resulting from the destruction of unconjugated bilirubin, the great part through the placenta into the maternal circulation to remove. it just newborns are born without jaundice. After birth, newborns must deal with their own hemoglobin metabolites a unconjugated bilirubin. But glucuronic acid transferase in full-term infants to 3 ~ 5 days, premature infants to 5 ~ 7 days maturity. Impose outlined already mentioned in the various neonatal bilirubin metabolism, it happened physiological neonatal jaundice. A clinical performance. Physiological jaundice were lightly yellow light confined to the face and neck, or spread to the trunk, sclera or yellow, 2 ~ 3 dissipated future, to 5 ~ on the 6th resume normal skin color; severe jaundice in the vanguard after the same foot the entire body. vomitus and cerebrospinal fluid and so on, can be stained, lasted more than a week, especially in premature infants sustainable individual to four weeks. its still-yellow fecal and urine without bilirubin. 2. Light color of jaundice were lightly color, the deeper the color is severe, but ruddy skin, yellow Lane rosy. 3. Jaundice were mostly observed in the trunk, sclera and proximal limbs However Zhouxi general. 4. Newborn generally good, without anemia, liver and spleen is not enlarged, normal liver function, the non-occurrence of jaundice. 5. Premature infants physiological jaundice than full-term infants were frequently seen, a slightly delayed ~ 2d emergence of a heavier degree of jaundice, have dissipated later, can be extended to 2 ~ 4 weeks. Diagnosis (1) a history. Jaundice times within a 24-hour common jaundice should be the first consideration of hemolytic disease of newborns. Next, consider other congenital CMV infection; 2 ~ 3 days to those physiological jaundice most common ABO hemolytic disease should be the exception; 4 ~ 7 days were to sepsis, breast milk jaundice see more; Seven days later they were showing jaundice sepsis, neonatal pneumonia. biliary atresia, breast milk jaundice is possible. 2. The rapid development of neonatal jaundice hemolytic disease of the fastest, followed by the most sepsis, neonatal hepatitis and biliary atresia slower development and lasting. 3. Feces and urine color to the color of soiled very shallow or gray urine indicates the deep neonatal hepatitis or biliary atresia. 4. Family is family history of Vicia faba patients should consider whether G6PD deficiency; Parents should hepatitis except hepatitis. 5. Pregnancy history, production history (PROM, suggested extending the middle-class when infection), perinatal mothers before medication history. (2) stool obviously pigment should consider neonatal hemolytic disease and septicemia. For performance poisoning infection, should be carried out blood, urine culture. 2. For hemolytic performance (reticulated cells increased, nucleated red blood cells "10/100 interleukin-2), maternal and child should check the ABO and Rh blood group, the anti-human globulin is a person who tests positive Rh blood group incompatibility; ABO hemolytic disease of infants antibody release test positive. These tests were negative birth or three, four days before onset should except G6PD deficiency. (C) almost no fecal bile pigment urine profound, positive urine bilirubin should consider neonatal hepatitis and biliary atresia, The former is often caused by long-standing fundamental than completely intrahepatic obstruction, the two identification more difficult, the following checks for reference. 1. Determination of serum bilirubin repeatedly suggested gradually increased biliary atresia, if irregular fluctuations or drop suggest hepatitis. 2. Early serum transaminase marked entrance examination suggest hepatitis. 3. Other laboratory tests of serum 5'-nucleotidase activity increased significantly suggest biliary atresia; Serum alpha-fetoprotein "40 mg / L suggest hepatitis; duodenal fluid containing bile acid can be reduced or extrahepatic biliary atresia; Lipoprotein-X (LP-X) were positive suggest biliary atresia. 4. Intravenous injection of 131I rose 37 ~ metastases (1 ~ 4μCi) three days to collect stool (not mixed with urine) test every minute counts, such as "10% of the injected dose can be excluded from biliary atresia. 5. Radionuclide liver, biliary scanning injection of 99m Tc-labeled ammonia acetate (IDA) derivatives after scanning, Children with hepatitis liver uptake has been slow and there intestinal radioactive concentration, the liver of patients with biliary atresia enhancement emerging fast, Intestinal there is no enhancement. 6.B-General can be found biliary cyst, in the absence of gallbladder suggest biliary atresia. 7. Liver biopsy basic structure of the normal liver, bile duct proliferation suggest biliary atresia; The same was true structural disorder and Liver cell necrosis, multinucleated giant cells suggest hepatitis easy to find. 8. Laparotomy for the two months purposes, in the absence of the gallbladder to further exploration; For gallbladder, should Cholecystography. If it abnormal liver-jejunostomy (implemented sooner the better, but not later than 3 months).