Information on Jaundice
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By :
peter hutch
Submitted
2008-05-29 00:00:00 |
Neonatal jaundice may have first been described in a Chinese textbook 1000 years ago. Medical theses, essays, and textbooks from the 18th and 19th centuries contain discussions about the causes and treatment of neonatal jaundice. Several of these texts also describe a lethal course in infants who probably had Rh isoimmunization. In 1875, Orth first described yellow staining of the brain, in a pattern later referred to as kernicterus.
Neonatal jaundice, although a normal transitional phenomenon in most infants, can occasionally become more pronounced. Blood group incompatibilities (eg, Rh, ABO) may increase bilirubin production through increased hemolysis.
Jaundice comes from the French word jaune, which means yellow. When it is said that a baby is jaundiced, it simply means that the color of his skin appears yellow. Jaundice in the infant appears first in the face and upper body and progresses downward toward the toes. Premature infants are more likely to develop jaundice than full-term babies.
Jaundice is a condition of excessive build up of a substance called bilirubin in the blood. Bilirubin is a product of break down of red blood cells and is normally processed by the liver and excreted from the body in bile. When the liver malfunctions, bilirubin is not excreted and it gets deposited near the skin surface giving a yellow tinge to the skin, mucous membranes, and eyes.
Baby jaundice is caused because soon after birth, baby's liver is not efficient enough to dispose off a yellow pigment called bilirubin, formed by normal metabolic breakdown of hemoglobin in the red blood cells. As a result, bilirubin accumulates in the blood giving yellowish appearance to baby’s skin and eyes. Most of the babies do not require a treatment of jaundice, as it tends to clear up on its own when baby’s liver starts functioning efficiently.
Jaundice is a common clinical problem in neonatal period which may result in brain damage even in healthy full term newborns, when it is severe. The aim of this study was to characterize the therapeutic effect of clofibrate in full term neonates who present with nonhemolytic jaundice.
A newborn's liver is immature and cannot process bilirubin as quickly as he will be able to when he gets older. This slow processing of bilirubin has nothing to do with liver disease. It merely means that the baby's liver is not as fully developed as it will be, and thus, there is some delay in eliminating the bilirubin.
Hyperbilirubinemia in newborns is primarily due to immaturity of the liver enzyme system (see box below). Jaundice can be classified as physiologic or nonphysiologic according to postdelivery timing of onset, clinical course, resolution, rate of bilirubin increases, and total serum bilirubin levels.
Physiologic jaundice and breast-milk jaundice usually do not cause problems for the infant; however, there is a concern that high or prolonged elevations in levels of unconjugated bilirubin (the type of bilirubin that is not attached to glucuronic acid and the main type of bilirubin that is present in physiologic and breast-milk jaundice) will cause neurologic damage to the infant. Therefore, when unconjugated bilirubin levels are high or prolonged, treatment usually is started to lower the levels of bilirubin.
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