hyperbilirubinemia /hy·per·bil·i·ru·bin·emia/ (-bil″ĭ-roo″bĭ-ne´me-ah) excess of bilirubin in the blood; classified as conjugated or unconjugated, according to the predominant form of bilirubin present.
Hyperbilirubinemia
hyperbilirubinemia
hyperbilirubinemia [hi″per-bil″ĭ-roo″bĭ-ne´me-ah]
hyperbilirubinemia
hyperbilirubinemia
hy·per·bil·i·ru·bi·ne·mi·a (h  p r-b l-r b-n  m-)n. An abnormally high concentration of bilirubin in the blood. |
Hyperbilirubinemia
A condition where there is a high level of bilirubin in the blood. Bilirubin is a natural by-product of the breakdown of red blood cells, however, a high level of bilirubin may indicate a problem with the liver.
Mentioned in: Erythroblastosis Fetalis, Hereditary Fructose Intolerance
hyperbilirubinemia
[hī′pərbil′iro̅o̅′binē′mē·ə]
Etymology: Gk, hyper + L, bilis, bile, ruber, red; Gk, haima, blood
greater than normal amounts of the bile pigment bilirubin in the blood, often characterized by jaundice, anorexia, and malaise. Hyperbilirubinemia is most often associated with liver disease or biliary obstruction, but it also occurs when there is excessive destruction of red blood cells, as in hemolytic anemia. Treatment is specific to the underlying condition. When bilirubin levels are high, treatment includes phototherapy and hydration. Also spelled hyperbilirubinaemia. See also jaundice.
hyperbilirubinemia [hi″per-bil″ĭ-roo″bĭ-ne´me-ah]
an excess of bilirubin in the blood, occurring as a result of liver or biliary tract dysfunction or with excessive destruction of red blood cells. It is classified as conjugated or unconjugated, according to the type of bilirubin present. Jaundice is manifested when excess bilirubin is deposited in the skin and mucous membranes.
hyperbilirubinemia I Gilbert disease.
hyperbilirubinemia II a chronic idiopathic jaundice, transmitted as an autosomal recessive trait, that affects the excretory function of the liver. The resulting increase in serum conjugated bilirubin is caused by defective transport of conjugated bilirubin into the biliary tract. The condition is generally harmless. Called also Dubin-Johnson syndrome.
conjugated hyperbilirubinemia, Type III a form of conjugated hyperbilirubinemia; probably the result of a primary defect in the storage or hepatic uptake of bilirubin.
hyperbilirubinemia in the newborn excess serum bilirubin in the newborn due either to overproduction of bilirubin, as in excessive destruction of erythrocytes, or to reduction in glucuronide conjugation in the liver. If a high level of bilirubinemia is left untreated, kernicterus may occur as a result of free unconjugated bilirubin entering the brain tissue and causing neurotoxic damage. The exact level at which kernicterus will occur in individual newborns has not been established. There is evidence that bilirubin levels as low as 6 to 9 mg/dl in very-low-birth-weight and preterm infants puts them at risk for kernicterus and brain damage.
Treatment. The goal of therapy is to reduce serum bilirubin and prevent kernicterus, which virtually disappears when bilirubin levels are controlled. Phototherapy is the standard treatment for nonhemolytic hyperbilirubinemia. It may be used prophylactically in newborns at high risk, for example, in preterm, low-birth-weight, and very-low-birth-weight newborns. Exchange transfusions are used for treatment of moderate to severe hemolytic disease, or when excessive bilirubinemia in preterm newborns is not controlled by phototherapy.
Patient Care. Newborns most at risk for hyperbilirubinemia are those who are preterm, who display bruising, or who have blood incompatibilities, an enclosed hemorrhage such as cephalhematoma, polycythemia, an intrauterine infection, congenital red blood cell abnormality, or congenital hypothyroidism or galactosemia.
Observation of the newborn for jaundice is of primary importance, especially those predisposed to hyperbilirubinemia. Yellowing of the skin is first apparent on the face, progressing downward as it increases in severity. The time at which jaundice is first noticed also is significant. Laboratory data can provide information on the levels of direct and indirect serum bilirubin, the hematocrit, variations in red cell morphology, reticulocyte count, Coombs' test and crossmatching of the infant's cells and maternal serum to detect abnormal antibodies when infant and mother are of the same blood type, and special tests for enzyme deficiencies and galactosemia.
Clinical jaundice is investigated when the jaundice appears in the first 12 hours of life and serum bilirubin levels rise at the rate of more than 3 mg per hour. These signs are indicative of hemolytic jaundice, which may require an exchange transfusion. Physiologic jaundice, which is due to immature liver function, rarely becomes apparent before the third day of life or persists beyond the first week and does not exceed 12 mg in term infants.
Other observations include noting any bruising, which causes hemolysis of erythrocytes and release of the bilirubin component, and assessment for cephalhematoma, which has the same effect as bruising because accumulated red blood cells are broken down. Intestinal obstruction also can lead to a buildup of serum bilirubin. The unevacuated stool contains bile which is broken down by intestinal flora into its basic components, thus allowing the release of bilirubin into the blood stream.
Care of the newborn receiving phototherapy includes protection of the skin and eyes from ultraviolet radiation. Care of the newborn receiving an exchange transfusion is discussed under that topic.
Observation of the newborn for jaundice is of primary importance, especially those predisposed to hyperbilirubinemia. Yellowing of the skin is first apparent on the face, progressing downward as it increases in severity. The time at which jaundice is first noticed also is significant. Laboratory data can provide information on the levels of direct and indirect serum bilirubin, the hematocrit, variations in red cell morphology, reticulocyte count, Coombs' test and crossmatching of the infant's cells and maternal serum to detect abnormal antibodies when infant and mother are of the same blood type, and special tests for enzyme deficiencies and galactosemia.
Clinical jaundice is investigated when the jaundice appears in the first 12 hours of life and serum bilirubin levels rise at the rate of more than 3 mg per hour. These signs are indicative of hemolytic jaundice, which may require an exchange transfusion. Physiologic jaundice, which is due to immature liver function, rarely becomes apparent before the third day of life or persists beyond the first week and does not exceed 12 mg in term infants.
Other observations include noting any bruising, which causes hemolysis of erythrocytes and release of the bilirubin component, and assessment for cephalhematoma, which has the same effect as bruising because accumulated red blood cells are broken down. Intestinal obstruction also can lead to a buildup of serum bilirubin. The unevacuated stool contains bile which is broken down by intestinal flora into its basic components, thus allowing the release of bilirubin into the blood stream.
Care of the newborn receiving phototherapy includes protection of the skin and eyes from ultraviolet radiation. Care of the newborn receiving an exchange transfusion is discussed under that topic.
hyperbilirubinemia
(hī´p
rbil´ēroo´-binē´mē),
n a greater than normal amounts of the bile pigment bilirubin in the blood, often characterized by jaundice, anorexia, and malaise. It is associated with liver disease and biliary obstruction, but it also occurs when there is excessive destruction of red blood cells, as in hemolytic anemia.
rbil´ēroo´-binē´mē), n a greater than normal amounts of the bile pigment bilirubin in the blood, often characterized by jaundice, anorexia, and malaise. It is associated with liver disease and biliary obstruction, but it also occurs when there is excessive destruction of red blood cells, as in hemolytic anemia.
hyperbilirubinemia
excess of bilirubin in the blood; classified as conjugated or unconjugated according to the form of bilirubin present. See also jaundice.
congenital hyperbilirubinemia
see gilbert's syndrome.
hyperbilirubinemia
Hepatology An ↑ of BR in the peripheral circulation; BR is either unconjugated, or conjugated to glucuronic acid, which ↑ BR's water solubility and facilitates its entry into the bile; hyperbilirubinemia in
neonates is due to ↓ metabolism, clearance, and liver immaturity. See Jaundice.
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