Chapter 38 Hyperbilirubinemia
PATHOPHYSIOLOGY
Neonatal hyperbilirubinemia or physiologic jaundice, a total serum bilirubin level higher than 5 mg/dl, is due to the neonate’s predisposition for bilirubin production and limited ability to excrete it. By definition, there is no other abnormality or pathologic process present to account for the jaundice. The yellow coloration of the skin and mucous membranes is due to the deposition of unconjugated bilirubin pigment. The primary source of bilirubin is the breakdown of hemoglobin in aging or hemolyzed red blood cells (RBCs). In the neonate, RBCs have a higher turnover and a shorter life span, which enhances the higher production rate of bilirubin. The immaturity of the neonatal liver is a limiting factor in bilirubin excretion.
Unconjugated or indirect bilirubin is lipid soluble and binds to plasma albumin. The bilirubin is then taken up by the liver, where it is conjugated. Conjugated or direct bilirubin is excreted in the bile into the intestines. In the intestines, bacteria convert the conjugated bilirubin into urobilinogen. The majority of the highly soluble urobilinogen is reexcreted by the liver and is eliminated in the feces; the kidneys excrete 5% of the urobilogen. Not only do increased RBC destruction and liver immaturity promote increased bilirubin levels, but other intestinal bacteria can deconjugate bilirubin, which allows it to be reabsorbed into the circulation and further raises bilirubin levels.
INCIDENCE
1. Up to 60% of term newborns have clinical evidence of jaundice.
2. Age of onset is 2 to 3 days.
3. Severity differs among different races, with Asian and Native American infants manifesting higher bilirubin levels.
4. Infants from certain geographic areas, particularly areas around Greece, have an increased incidence of hyperbilirubinemia.
5. Birth trauma (cephalohematoma, cutaneous bruising, instrumented delivery) increases risk for hyperbilirubinemia.
MEDICAL MANAGEMENT
Medical management is largely supportive. Prevention of neonatal hyperbilirubinemia should always be attempted by initiating feedings as soon as possible after birth. Bilirubin levels should be monitored, and the infant will be placed under phototherapy as the blood level dictates. All other causes of hyperbilirubinemia should be ruled out at this time. Other causes include Rh incompatibility, hemolytic disease, and biliary atresia. Infants at high risk for developing hyperbilirubinemia, such as premature infants and those with hypoxia and acidosis, may be placed under phototherapy before developing a significantly elevated bilirubin level.
NURSING ASSESSMENT
NURSING INTERVENTIONS
1. Introduce feedings as soon as possible after birth as preventive measure.
3. During phototherapy do the following:
4. Administer glycerin suppository as needed to facilitate elimination of direct bilirubin in stool.
5. Promote bonding by encouraging parent to hold and feed infant while under phototherapy.
Ip S, et al. An evidence-based review of important issues concerning neonatal hyperbilirubinemia. Pediatrics. 2006;114:e130–e153. (serial online) www.pediatrics.org/cgi/content/full/114/1/e130 Accessed January 4
James SR, et al. Nursing care of children: principles and practice, ed 3. Philadelphia: WB Saunders, 2007.
Porter ML, Dennis RL. Hyperbilirubinemia in the term newborn. Am Fam Physician. 2002;64:599.
