الفهرس 
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Abstract
Neonatal jaundice has been known Si nce the golden age of classical medicine in Greece, Rome and Arabian peninsula, it was described before as being physiological process. Thereafter the types of neonatal jaundice and its different aetiology were clarified year by year.
Neonatal jaundice is one of the most frequent disorders confronted by the pediatricians. Approximately
25-SW& of the normal newborn population are visibly
jaudiced during the first week of life and a higher
percentage in the prematures, having a total serum bilirubin of greater than 7 mg/dl . Of these only a few have true pathol ogic jaundice,the majority have physiologic hyperbilirubinei. Therefore, it is important for the paediatricjan to develop a consistent approach to the investigation and management of the jaundiced newborn (Maisel s,1981).
Not only is the newborn unique because of his limited ability to clear bilirubin from the plasma,but also because (with rare exceptions) the newborn period remains the only time at which an elevated plasma bilirubin level per se represents a threat to the well being of the organi sm. The word JAUNDICE is derived from the French “JAUNE”, which means “yellow”. The yellow pigment was first isolated by Virchow in 1847, named [3ILIRUBIN by Staedeler in 1864. It’s structure determined by Siedel
& Fischer in 1933 & confirmed by total synthesis by
Fischer & Plieninger in 1943 & more recently by Plieninger et. al . Jaundice is yellow colour of the skin,conjunctiva, and other tissues caused by the presence of an excess of bilirubin in the plasma and tissue fluids.
Recent advances i n our knowl edge of the physi ol ogy and organic chemistry of bilirubin excretion have made possible a much clearer understanding of the pathogenesis and effects of neonatal jaundice.
Jaundice should be consi dered a sign of risk for the infant with the degree of danger that it may represent, dependent upon factors that affect the production, metabolism, excretion and distribution of bilirubin after birth. The newborn infant’s metabolism of bilirubin is in transition from, the foetal stage, when the placenta is the principal route of elimination of the lipid—soluble bilirubin, to the adult stage, when the water-soluble conjugated form i s excreted from the hepatic cell into the biliary system and then the gastrointestinal tract. Any factor that increases the load of bilirubin to be metabolised by the liver, or damages or reduce the activity of the enzyme, or competes for decreased amounts of the enzyme or reduction of builirubin uptake by the liver cell nay cause or increase the degree of jaundice C3ehrman and Kleigmanj983).