新生儿疾病-Neonatal Jaundice lwz英文课件

Neonatal Jaundice,站,Introduction,Neonatal Jaundice is known as the visible clinical manifestation of dying skin and sclera yellow during the neonatal period, resulting from deposition of bilirubin in the neonatal bodies.,Introduction,Jaundice is observed during the 1st wk in approximately 60% of term infant and 80% of preterm infant. Hyperbilirubinemia can be toxic, with high levels resulting in an encephalopathy known as kerni-cterus.,Metabolism of Bilirubin,Increased bilirubin production Less effective binding and transportation Less efficient hepatic conjugation Enhanced absorption of bilirubin via the enterohepatic circulation,Clinical Manifestation,Jaundice may be present at birth or at any time during the neonatal period. Jaundice usually begins on the face and, as the serum level increases, progresses to the chest and abdomen and then the feet. Jaundice resulting from deposition of indirect bilirubin in the skin tends to appear bright yellow or orange; jaundice of the obstructive type (direct bilibrubin), a greenish or muddy yellow.,Methods of Diagnosis,A complete diagnostic evaluation Determination of direct and indicrect bilirubin fractions Determination of hemoglobin Reticulocyte count Blood type Coombs test Examination of the peripheral blood smear,Classifications,Direct-reacting hyperbilirubinemia Hepatitis Cholestasis Inborn errors of metabolism Sepsis,Classifications,Indirect-reacting hyperbilirubinemia Hemolysis Reticulocytosis Evidences of red blood cell destruction A positive Coombs test Blood group incompatibility Positive results of specific examination,Classifications,Direct and indirect- reactin hyperbilirubinemia Hepatitis Sepsis Liver damage complicated by Hemolysis,Classifications,Physiologic jaundice Clinical jaundice appears at 2-3 days. Total bilirubin rises by less than 5 mg/dl (86 umol/L) per day. Peak bilirubin occurs at 3-5 days of age. Peak bilirubin concentration in Full-term infant 12mg/dl (205.2 umol/L) Peak bilirubin concentration in Premature infant 15mg/dl (257umol/L) Clinical jaundice is resolved by 2 weeks in the term infant by 3-4 weeks in the Preterm infant.,Classifications,Pathologic jaundice Clinical jaundice appears in 24 hours of age. Total bilirubin rises by higher than 5 mg/dl (86 umol/L) per day. Peak concentration of total bilirubin is more than 12 mg/dL in the term infant and 15 mg/ dL in the preterm infant.,Classifications,Pathologic jaundice Clinical jaundice is not resolved in 2 weeks in the term infant and in 4 weeks in the Preterm infant. Clinical jaundice appears again after it has been resolved. Direct bilirubin concentration is more than 1.5 mg/dL (26umol/L).,Causes of Pathologic Jaundice,Infective jaundice Neonatal hepatitis TORCH infection Neonatal sepsis,Causes of Pathologic Jaundice,Jaundice associated without infection Hemolytic disease of the newborn ABO incompatibility Rh incompatibility Biliary atresia Jaundice associated with breast- feeding,Causes of Pathologic Jaundice,Breast milk jaundice It is caused by prolonged increased enterohepatic circulation of bilirubin. (-GD) The hyperbilirubinemia peaks at 10-15 days of age. The level of unconjugated hyperbilirubinemia is at 10-30 mg/dL (172-516 umol/L). If nursing is interrupted for 72 hours, the bilirubin level falls quickly.,Causes of Pathologic Jaundice,Genetic disease Congenital deficiencies of the enzymes glucose-6-phosphate dehydrogenase (G-6-PD) Thalassemia Cystic fibrosis Drug Vitamin k Novobiocin,Hemolytic Disease of the Newborn,Li weizhong,Introduction,Hemolytic disease of the newborn It is an isoimmunity hemolysis associated with ABO or Rh incompatibility. It results from transplacental passage of maternal antiboddy active against RBC antigens of the infant, leading to an increased rate of RBC destruction. It is an important cause of anemia and jaundice in newborn infant.,Etiology and Pathogenesis,ABO hemolytic disease ABO incompatibility Type O mothers Type A or B fetuses Presence of IgG anti-A or Anti-B antibodies in type O mother Frequently occurring during the first pregnancy without prior sensitization,站,Etiology and Pathogenesis,Rh hemolytic disease Rh blood group antigens (C, c, D, d, E, e) DECce Pathophysiology of alloimmune hemolysis resulting from Rh incompatibility An Rh-negative mother An Rh-positive fetus Leakage of fetal RBC into maternal circulation Maternal sensitization to D antigen on fetal RBC,Etiology and Pathogenesis,Production and transplacental passage of maternal anti-D antibodies into fetal circulation Attachment of maternal antibodies to Rh-positive fetal RBC Destruction of antibody-coated fetal RBC,Etiology and Pathogenesis,Rh hemolytic disease was rare during the first pregnancy involving an Rh-positive fetus. Once sensitization has occurred, re-exposure to Rh D RBC in subsequent pregnancies leads to an anamnestic response, with an increase in the maternal anti-Rh D antibody titer. The likelihood of an infant being affected increased significantly w