Hyperbilirubinemia, also called neonatal jaundice, is the result of hemolytic processes in the neonate. It’s marked by elevated serum bilirubin levels and mild jaundice and can be physiologic (with jaundice the only symptom) or pathologic (resulting from an underlying disease). Physiologic jaundice tends to be more common and more severe in certain ethnic groups (Chinese, Japanese, Koreans, Native Americans), whose mean peak of unconjugated bilirubin is approximately twice that of the rest of the population. Physiologic jaundice is self-limiting; the prognosis for pathologic jaundice varies, depending on the cause.
Untreated, severe hyperbilirubinemia may result in kernicterus, a neurologic syndrome resulting from deposition of unconjugated bilirubin in the brain cells and characterized by severe neural symptoms. Survivors may develop cerebral palsy, epilepsy, or mental retardation or have only minor sequelae, such as perceptual-motor handicaps and learning disorders.
As erythrocytes break down at the end of their neonatal life cycle, hemoglobin (Hb) separates into globin (protein) and heme (iron) fragments. Heme fragments form unconjugated (indirect) bilirubin, which binds with albumin for transport to liver cells to conjugate with glucuronide, forming direct bilirubin. Because unconjugated bilirubin is fat-soluble and can’t be excreted in the urine or bile, it may escape to extravascular tissue, especially fatty tissue and the brain, resulting in hyperbilirubinemia.
This pathophysiologic process may develop when:
❑ certain factors disrupt conjugation and usurp albumin-binding sites, including drugs (such as aspirin, tranquilizers, and sulfonamides) and conditions (such as hypothermia, anoxia, hypoglycemia, and hypoalbuminemia)
❑ decreased hepatic function results in reduced bilirubin conjugation
❑ increased erythrocyte production or breakdown results from hemolytic disorders, or Rh or ABO incompatibility
❑ biliary obstruction or hepatitis results in blockage of normal bile flow
❑ maternal enzymes present in breast milk inhibit the neonate’s glucuronyl-transferase conjugating activity. (See Causes of hyperbilirubinemia, page 986.)
The primary sign of hyperbilirubinemia is jaundice, which doesn’t become clinically apparent until serum bilirubin levels reach about 7 mg/dl. Physiologic jaundice develops 24 hours after delivery in 50% of term neonates (usually day 2 to day 3) and 48 hours after delivery in 80% of premature neonates (usually day 3 to day 5). It generally disappears by day 7 in term neonates and by day 10 in premature neonates. Throughout physiologic jaundice, serum unconjugated bilirubin levels don’t exceed 12 mg/dl. Pathologic jaundice may appear anytime after the first day of life and persists beyond 7 days with serum bilirubin levels greater than 12 mg/dl in a term neonate, 15 mg/dl in a premature neonate, or increasing more than 5 mg/dl in 24 hours.
Inspection of the neonate in a well-lit room (without yellow or gold lighting) reveals yellowish skin coloration, particularly in the sclerae. Jaundice can be verified by pressing the skin on the cheek or abdomen lightly with one finger, then releasing pressure and observing skin color immediately. Signs of jaundice necessitate measuring and charting serum bilirubin levels every 4 hours. Testing may include direct and indirect bilirubin levels, particularly for pathologic jaundice. Bilirubin levels that are excessively elevated or vary daily suggest a pathologic process.
Identifying the underlying cause of hyperbilirubinemia requires a detailed patient history (including prenatal history), family history (paternal Rh factor, inherited red cell defects), present neonate status (immaturity, infection), and blood testing of the neonate and mother (blood group incompatibilities, Hb levels, direct Coombs’test, hematocrit).
Depending on the underlying cause, treatment may include phototherapy, exchange transfusions, albumin infusion and, possibly, drug therapy. Phototherapy is the treatment of choice for physiologic jaundice, and pathologic jaundice due to erythroblastosis fetalis (after the initial exchange transfusion). Phototherapy uses fluorescent light to decompose bilirubin in the skin by oxidation and is usually discontinued after bilirubin levels fall below 10 mg/dl and continue to decrease for 24 hours. However, phototherapy is rarely the only treatment for jaundice due to a pathologic cause.
An exchange transfusion replaces the neonate’s blood with fresh blood (less than 48 hours old), removing some of the unconjugated bilirubin in serum. Possible indications for exchange transfusions include hydrops fetalis, polycythemia, erythroblastosis fetalis, marked reticulocytosis, drug toxicity, and jaundice that develops within the first 6 hours after birth.
Other therapy for excessive bilirubin levels may include albumin administration (1 g/kg of 25% salt-poor albumin), which provides additional albumin for binding unconjugated bilirubin. This may be done 1 to 2 hours before exchange or as a substitute for a portion of the plasma in the transfused blood.
Drug therapy, which is rare, usually consists of phenobarbital administered to the mother before delivery and to the neonate several days after delivery. This drug stimulates the hepatic glucuronide-conjugating system.
❑ Assess and record the neonate’s jaundice, and note the time it began. Report the jaundice and serum bilirubin levels immediately.
❑ Reassure parents that most neonates experience some degree of jaundice. Explain hyperbilirubinemia, its causes, diagnostic tests, and treatment. Also, explain that the neonate’s stool contains some bile and may be greenish.
For the neonate receiving phototherapy:
❑ Keep a record of how long each bilirubin light bulb is in use because these bulbs require frequent changing for optimum effectiveness.
❑ Undress the neonate, so his entire body surface is exposed to the light rays. Keep him 18" to 30"(46 to 76 cm) from the light source. Protect his eyes with shields that filter the light.
❑ Monitor and maintain the neonate’s body temperature; high and low temperatures predispose him to kernicterus. Remove the neonate from the light source every 3 to 4 hours and take off the eye shields. Allow his parents to visit and feed him.
❑ The neonate usually shows a decrease in serum bilirubin level 1 to 12 hours after the start of phototherapy. When the neonate’s bilirubin level is less than 10 mg/dl and has been decreasing for 24 hours, discontinue phototherapy as ordered. Resume therapy, as ordered, if serum bilirubin increases several milligrams per deciliter, as it often does because of a rebound effect.
For the exchange transfusions:
❑ Prepare the neonate warmer and tray before the transfusion. Try to keep the neonate quiet. Give him nothing by mouth for 3 to 4 hours before the procedure.
❑ Check the blood to be used for the exchange — type, Rh, age. Keep emergency equipment (resuscitative and intubation equipment, and oxygen) available. During the procedure, monitor respiratory and heart rates every 15 minutes; check the neonate’s temperature every 30 minutes. Continue to monitor vital signs every 15 to 30 minutes for 2 hours.
❑ Measure intake and output. Observe for cord bleeding and complications, such as hemorrhage, hypocalcemia, sepsis, and shock. Report serum bilirubin and Hb levels. Bilirubin levels may rise, as a result of a rebound effect, within 30 minutes after transfusion, necessitating repeat transfusions.
To prevent hyperbilirubinemia:
❑ Maintain oral intake. Don’t skip any feedings, because fasting stimulates the conversion of heme to bilirubin.
❑ Administer Rho(D) immuneglobulin (human), as ordered, to an Rh-negative mother after amniocentesis, or — to prevent hemolytic disease in subsequent infants — to an Rh-negative mother during the third trimester, after the birth of an Rh-positive neonate, or after spontaneous or elective abortion.
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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
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