新生儿黄疸（英文）.ppt

Neonatal Jaundice Introduction All babies develop elevated serum bilirubin (SBR) levels, to a greater or lesser degree, in the first week of life. This is due to: increased production (accelerated RBC breakdown); decreased removal (liver enzyme insufficiency) Increased reabsorption (enterohepatic circulation). Introduction ~60% of infants become clinically jaundiced in 1st wk Bili levels peak at 3~5 days in full term infants ~1/6 of formula fed infants have bili levels over 12 ~1/3 of breast fed infants have bili levels over 12 Over 80% of all infants with bili levels12.9 mg/dl in the first four days of life are breast fed Bilirubin Metabolism derived from the catabolism of proteins that contain heme the most important source is the breakdown of Hb from RBC native bilirubin is relatively insoluble in water at physiologic pH, but it is very lipid soluble bilirubin circulates bound to albumin in equilibrium with its unbound or free fraction the unbound fraction that readily crosses the blood-brain barrier and results in neurotoxicity Bilirubin Metabolism Bilirubin is made more water-soluble in the liver by conjugation with glucuronic acid to form conjugated or direct-reacting bilirubin, then cleared through the bile into the intestines and out through the feces. Phototherapy works by producing photoisomers of bilirubin that are more water soluble, and that can be cleared directly in bile or urine without conjugation in the liver. “enterohepatic circulation”: b-glucuronidase in the gut hydrolysis the conjugated bilirubin into unconjugated bilirubin, and reabsorbed into liver Characteristics of Neonatal Bilirubin Metabolism Increased bilirubin production 8.8mg/kg daily vs 3.8mg/kg in adults Insufficiency of bilirubin transportation acidosis, hypoalbuminemia Immature of liver function lower ingestion (y, z protein); lower UDPGT activity Increased “enterohepatic circulation” lower in gut