Neonatal Jaundice Health Article

Definition

Neonatal jaundice and hyperbilirubinemia are terms used when a newborn has a higher-than-normal level of bilirubin in the blood. Bilirubin is an end-product of the breakdown of the hemoglobin present in the red blood cells at the end of their life cycle. Hemoglobin carries oxygen to tissues and cells. Before birth the placenta is not as efficient in providing oxygen as the baby's lungs will be after birth. Because of this, infants in utero have more red blood cells than they will need after birth to provide enough oxygen. Therefore, newborns have an excess of red blood cells that they need to process, and an immature liver with which to complete the job. Jaundice refers to the yellow discoloration of the skin and sclera (whites) of the eyes, which results as the breakdown of bilirubin goes faster than the rate at which it can leave the body, causing its level to rise in the blood.

Description

When the fetus is in utero, bilirubin is processed through the placenta and the maternal-fetal circulation. After birth, the infant's often-immature liver must take over this task. Clinical jaundice (serum bilirubin levels of 5-7 mg/dL and above) occurs in about 60-70% of term newborns, and about 80% of premature infants. Ever since hospital stays after delivery decreased to 24-48 hours postpartum, hyperbilirubinemia has become the leading cause of hospital readmissions in the first two weeks of life. The greatest concern with hyperbilirubinemia is that the unexcreted bilirubin will begin to deposit in the brain of the neonate, resulting in a serious, potentially life-threatening condition called kernicterus. Another term used for kernicterus is brain encephalopathy.

Causes and symptoms

An elevated bilirubin level may be due to its increased production, a decreased rate of conjugation, or abnormalities of the liver. In order for the bilirubin to be excreted in the urine and stool, it must be converted, or conjugated from a fat- or lipid-soluble form to a water-soluble form. Bilirubin that has not been excreted can be reabsorbed and contributes to increased blood levels.

Initial symptoms of a rising bilirubin level can be subtle, and usually include increased drowsiness, which leads to poor feeding, and the subsequent decreased urine and stool output. The diaper may contain orange spots, an indication of the presence of uric acid crystals, a sign of dehydration. A change in the infant's cry to a high-pitched tone may indicate early neurological damage.

There are several types of jaundice. The most common form of neonatal jaundice appears between the first 24-72 hours after birth and is usually considered a benign form. It is often referred to as early-onset breast milk jaundice, and is related to insufficient breastfeeding, which results in decreased nutritional intake and decreased stooling. With decreased stooling the bilirubin in the stool is not being excreted, and is also available for reabsorption. Increasing the feedings from six to 12 times a day, and checking for latching-on and a good suck and swallow pattern, can lead to a decreasing bilirubin level to within normal limits. To encourage adequate maternal milk production, supplementation with water or glucose is discouraged.

Late-onset breast milk jaundice may occur in 10-30% of breast-fed infants and appears in the second to sixth weeks of life. This form of jaundice is believed to be related to a substance present in the mother's milk that affects the infant's absorption of bilirubin.

Jaundice that sets in within the first 24 hours after birth is usually due to an Rh factor or ABO blood incompatibility between the mother and infant.

Risk factors for the development of hyperbilirubinemia include:

• premature birth
• Asian and Native American descent—including more rapid rise and higher peak levels of bilirubin
• maternal diabetes
• hemolytic disease in the neonate
• sepsis
• family history of jaundice
• presence of excessive bruising due to traumatic birth, and cephalhematoma
• oxytocin-induced delivery
• mother's use of sulfa medications during pregnancy
• history of familial liver disease
• delayed cord clamping
• thyroid gland abnormalities
• G6PD (glucose-6-phosphate dehydrogenase) deficiency

Diagnosis

Diagnosis of hyperbilirubinemia usually begins with the observation of jaundice at the time of physical examination. However, a delay in recognition of jaundice may occur since many infants have already gone home prior to its onset. Pediatric practices vary as to times of follow-up after hospital discharge. Parents may call their pediatric care provider's office because of jaundice, or because of a decreased ability of the infant to feed. Examination of the infant is best done next to a window so that the jaundice can be assessed in natural light. Blood tests to check the bilirubin level, blood type, and for signs of dehydration will usually be ordered.