hyperbilirubinemia of the newborn
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hyperbilirubinemia of the newborn
an excess of bilirubin in the blood of the neonate. It is usually caused by a deficiency of an enzyme that results from physiological immaturity or by increased hemolysis, especially that produced by blood group incompatibility, which, in severe cases, can lead to kernicterus. Also called neonatal hyperbilirubinemia. See also breast milk jaundice, cholestasis, Crigler-Najjar syndrome, Dubin-Johnson syndrome, erythroblastosis fetalis, Gilbert's syndrome, kernicterus, phototherapy in the newborn, Rotor's syndrome.
observations The elevation of serum bilirubin levels in the normal newborn is caused by the greater concentration of circulating erythrocytes and the infant's diminished ability to conjugate and excrete bilirubin because of a lack of the enzyme glucuronyl transferase, a reduced albumin concentration, and a lack of intestinal bacteria. Jaundice appears when blood levels of bilirubin exceed 5 mg/dL, usually not before 24 hours in full-term neonates. Clinically observable jaundice or serum bilirubin level exceeding 5 mg/dL within the first 24 hours of life is abnormal and indicates a pathological cause of hyperbilirubinemia. In erythroblastosis fetalis, jaundice is evident shortly after birth, and bilirubin levels rise rapidly. Severely affected infants also show hepatosplenomegaly and signs of anemia, which quickly worsen, causing a decrease in oxygen-carrying capacity that may lead to cardiac failure and shock. Early symptoms of kernicterus are lethargy, poor feeding, and vomiting, followed by severe neurological excitation or depression, including tremors, twitching, convulsion, opisthotonos, a high-pitched cry, hypotonia, diminished deep tendon reflexes, and absence of Moro and sucking reflexes. Brain damage generally does not occur at serum bilirubin levels below 20 mg/dl in an otherwise healthy term infant. Factors such as metabolic acidosis, lowered albumin levels, hypoxia, hypothermia, free fatty acids, and certain drugs, especially salicylates and sulfonamides, increase the risk at much lower levels. The mortality rate may reach 50%. Sequelae of kernicterus include mental retardation, minimal brain dysfunction, cerebral palsy, delayed or abnormal motor development, hearing loss, ataxia, athetosis, perceptual problems, and behavioral disorders.
interventions Such preventive measures as frequent feedings during the first 6 to 12 hours of life to increase GI motility have little justification. Infants with mild jaundice require no treatment, only observation. Phototherapy is the usual treatment for severe or increasing hyperbilirubinemia. If hyperbilirubinemia is the result of increased hemolysis caused by blood group incompatibility, exchange transfusion may be done. It is usually indicated if laboratory analysis reveals a positive antiglobulin test result, a hemoglobin concentration of the cord blood below 12 g/dl, or a bilirubin level of 20 mg/dl or more in a full-term infant or 15 mg/dl or more in a premature infant. Phototherapy may be used in conjunction with exchange transfusion, except in cases of Rh incompatibility. If used immediately after the initial exchange transfusion, phototherapy may remove enough bilirubin from the tissues to make subsequent transfusions unnecessary. Clinical practice nomograms using major and minor risk factors are useful for predicting worsening hyperbilirubinemia and need for phototherapy or exchange transfusion.
nursing considerations An initial concern is to identify high-risk infants in whom hyperbilirubinemia and kernicterus may develop. The nurse may monitor the serum bilirubin levels and observe for evidence of jaundice, anemia, central nervous system irritability, and such conditions as acidosis, hypoxia, and hypothermia. In erythroblastosis fetalis, exchange transfusion may be necessary. The amounts of blood infused and withdrawn, the vital signs, and any signs of exchange reactions are noted. Resuscitative equipment is kept available. Optimal body temperature is maintained: Hypothermia increases oxygen and glucose consumption, causing metabolic acidosis, and hyperthermia damages the donor's erythrocytes, causing an elevation in the amount of free potassium, which may lead to infant cardiac arrest. After the procedure a sterile dressing is applied to the catheter site.