neonatal jaundice

(redirected from non-pathologic unconjugated hyperbilirubinemia)

Neonatal Jaundice



Neonatal jaundice (or hyperbilirubinemia) is a higher-than-normal level of bilirubin in the blood. Bilirubin is a by-product of the breakdown of red blood cells. This condition can cause a yellow discoloration of the skin and the whites of the eyes called jaundice.


Bilirubin, a by-product of the breakdown of hemoglobin (the oxygen-carrying substance in red blood cells), is produced when the body breaks down old red blood cells. Normally, the liver processes the bilirubin and excretes it in the stool. Hyperbilirubinemia means there is a high level of bilirubin in the blood. This condition is particularly common in newborn infants. Before birth, an infant gets rid of bilirubin through the mother's blood and liver systems. After birth, the baby's liver has to take over processing bilirubin on its own. Almost all newborns have higher than normal levels of bilirubin. In most cases, the baby's systems continue to develop and can soon process bilirubin. However, some infants may need medical treatment to prevent serious complications which can occur due to the accumulation of bilirubin.

Causes and symptoms

In newborn infants, the liver and intestinal systems are immature and cannot excrete bilirubin as fast as the body produces it. This type of hyperbilirubinemia can cause jaundice to develop within a few days after birth. About one-half of all newborns develop jaundice, while premature infants are much more likely to develop it. Hyperbilirubinemia is also more common in some populations, such as Native American and Asian. All infants with jaundice should be evaluated by a health care provider to rule out more serious problems.
Hyperbilirubinemia and jaundice can also be the result of other diseases or conditions. Hepatitis, cirrhosis of the liver, and mononucleosis are diseases that can affect the liver. Gallstones, a blocked bile duct, or the use of drugs or alcohol can also cause jaundice.
Extremely high levels of bilirubin in infants may cause kernicterus, a form of brain damage. Signs of severe hyperbilirubinemia include listlessness, high-pitched crying, apnea (periods of not breathing), arching of the back, and seizures. If severe hyperbilirubinemia is not treated, it can cause mental retardation, hearing loss, behavior disorders, cerebral palsy, or death.


The initial diagnosis of hyperbilirubinemia is based on the appearance of jaundice at physical examination. The child is often placed by an open window so he/she may be checked in natural light. Blood samples may be taken to determine the bilirubin level in the blood.


Most cases of newborn jaundice resolve without medical treatment within two to three weeks, but should be checked by the health care provider. It is important that the infant is feeding regularly and having normal bowel movements. If bilirubin levels are extremely high, the infant may be treated with phototherapy—exposure of the baby's skin to fluorescent light. The bilirubin in the baby's skin absorbs the light and is changed to a substance that can be excreted in the urine. This treatment can be done in the hospital and is often done at home with special lights which parents can rent for the treatment. Treatment may be needed for several days before bilirubin levels in the blood return to normal. The baby's eyes are shielded to prevent the optic nerves from absorbing too much light. Another type of treatment uses a special fiberoptic blanket. There is no need to shield the baby's eyes with this treatment, and it can be done at home. In rare cases, where bilirubin levels are extremely high, the baby may need to receive a blood transfusion.


Most infants with hyperbilirubinemia and associated jaundice recover without medical treatment. Phototherapy is very effective in reducing bilirubin levels in the majority of infants who need it. There are usually no long-term effects on the child from the hyperbilirubinemia or the phototherapy. It is very rare that a baby may need a blood transfusion for treatment of this condition.


There is no way to predict which infants will be affected by hyperbilirubinemia. Newborns should be breastfed or given formula frequently, and feedings should begin as soon as possible after delivery to increase activity of the baby's digestive system.



D'Alessandro, Hellen Anne. Biliary Atresia. The Virtual Hospital Page. University of Iowa.
"Jaundice/Hyperbilirubinemia." 〈〉
"Jaundice in Newborn (Hyperbilirubinemia)."
"Neonatal Jaundice." 〈〉.
"Neonatology on the Web."

Key terms

Bilirubin — A yellowish-brown substance in the blood that forms as old red blood cells are broken down.
Hemoglobin — A protein, an oxygen-carrying pigment of the erythrocyte (red blood cell) formed in the bone marrow.
Jaundice — A yellow discoloration of the skin and whites of the eyes.
Kernicterus — A serious condition where high bilirubin levels cause brain damage in infants.


yellowness of skin, sclerae, mucous membranes, and excretions due to hyperbilirubinemia and deposition of bile pigments. It is usually first noticeable in the eyes, although it may come on so gradually that it is not immediately noticed by those in daily contact with the jaundiced person. Called also icterus.

Jaundice is not a disease; it is a symptom of a number of different diseases and disorders of the liver and gallbladder and of hemolytic blood disorders. One such disorder is the presence of a gallstone in the common bile duct, which carries bile from the liver to the intestine. This may obstruct the flow of bile, causing it to accumulate and enter the bloodstream. The obstruction of bile flow may cause bile to enter the urine, making it dark in color, and also decrease the bile in the stool, making it light and clay-colored. This condition requires surgery to remove the gallstone before it causes serious liver injury.

The pigment causing jaundice is called bilirubin. It is derived from hemoglobin that is released when erythrocytes are hemolyzed and therefore is constantly being formed and introduced into the blood as worn-out or defective erythrocytes are destroyed by the body. Normally the liver cells absorb the bilirubin and secrete it along with other bile constituents. If the liver is diseased, or if the flow of bile is obstructed, or if destruction of erythrocytes is excessive, the bilirubin accumulates in the blood and eventually will produce jaundice. Determination of the level of bilirubin in the blood is of value in detecting elevated bilirubin levels at the earliest stages before jaundice appears, when liver disease or hemolytic anemia is suspected.
Patient Care. Assessment of the patient with jaundice includes observations of the degree and location of yellowing, noting the color of urine and stools, and the presence of itching. Since jaundice can be accompanied by severe itching, frequent skin care is important to preserve skin integrity. Tepid sponge baths can help reduce discomfort and promote rest.

Patients with severe jaundice are at risk for encephalopathic changes that produce confusion, impaired mentation, and altered levels of consciousness. The potential for injury is increased and demands vigilance and safety measures to protect the patient.
Jaundice may be attributable to prehepatic (A), hepatic (B), or posthepatic (C) causes. From Damjanov, 2000.
acholuric jaundice jaundice without bilirubinemia, associated with elevated unconjugated bilirubin that is not excreted by the kidney. Familial acholuric jaundice is another name for the hereditary form of hemolytic jaundice.
breast milk jaundice elevated unconjugated bilirubin in some breast-fed infants due to the presence of an abnormal pregnane that inhibits glucuronyl transferase conjugating activity.
cholestatic jaundice that resulting from abnormality of bile flow in the liver.
familial nonhemolytic jaundice Gilbert disease.
hematogenous jaundice hemolytic jaundice.
hemolytic jaundice see hemolytic jaundice.
hepatocellular jaundice jaundice caused by injury to or disease of the liver cells.
leptospiral jaundice Weil's syndrome.
neonatal jaundice (jaundice of the newborn) icterus neonatorum.
nonhemolytic jaundice that due to an abnor-mality in bilirubin metabolism.
obstructive jaundice that due to blockage of the flow of bile.
physiologic jaundice mild icterus neonatorum during the first few days after birth.

phys·i·o·log·ic jaun·dice

a form of jaundice observed frequently in newborn infants in the first 1-2 weeks of life. It is caused by several factors, including a comparatively high red blood cell mass at birth compared with that of adults, shorter red blood cell lifespan, transiently impaired conjugation of bilirubin in the liver, and lack of gut flora (which are helpful in intestinal metabolism and excretion of bilirubin); is related to indirect (unconjugated) bilirubinemia that peaks at 2-3 days of age in normal, full-term infants and later with higher levels in preterm infants and is accentuated in breast-fed infants.

neonatal jaundice

neonatal jaundice

Yellowing of a newborn’s skin during the neonatal period, which is caused by an increased bilirubin level in the blood, due to immaturity of liver function plus destruction of red cells. Neonatal jaundice appears between days 2 and 5 and clears by 2 weeks, and is more common in premature infants.
Nonphysiologic, prolonged, or pathologic jaundice in newborn, biliary atresia, ABO and/or Rh incompatibility, galactosaemia, cephalhaematoma, polycythemia, G6PD deficiency, neonatal sepsis, congenital infection (CMV), toxoplasmosis, syphilis, herpes, rubella, late-pregnancy use of sulfa drugs by mother, Crigler-Najjar syndrome, hereditary spherocytosis, cystic fibrosis, breast-milk jaundice, pyruvate kinase deficiency, thalassaemia, Gilbert’s syndrome, congenital hypothyroidism, Lucey-Driscoll syndrome, Gaucher’s disease, Niemann-Pick disease.


pertaining to the period immediately after birth; the duration varies between species; in humans refers to the first four weeks of life; in animals the first week seems appropriate. Some neonatal disorders are listed in entries below. Others are listed elsewhere under titles specific to their anatomic location, including hyaline membrane disease, respiratory distress syndrome.

neonatal cardiac murmur
is observed in foals and most disappear before the fifth day. Persistence after that time may suggest valvular dysfunction. Many congenital murmurs are functional and cause no signs of disease.
neonatal diarrhea
see undifferentiated diarrhea of the newborn.
neonatal distress
see neonatal maladjustment syndrome (below).
neonatal edema
usually caused by obstruction to lymphatic flow by defective development of lymph drainage system.
neonatal hyaline membrane disease
see hyaline membrane disease.
neonatal hyperbilirubinemia
see neonatal jaundice (below).
neonatal hypoglycemia
a metabolic disease of newborn piglets caused by restriction of food intake. Clinical signs include weakness, shivering, hypothermia and terminal convulsions.
neonatal isoerythrolysis
see alloimmune hemolytic anemia of the newborn.
neonatal isoimmune purpura
see neonatal thrombocytopenic purpura (below).
neonatal jaundice
is an important clinical sign in foals because of the possibility of alloimmune hemolytic anemia. Some cases of benign, physiological jaundice also occur in foals. There is jaundice but no other clinical or pathological abnormality. Called also neonatal hyperbilirubinemia.
neonatal maladjustment syndrome
a disease of newborn thoroughbred foals caused by premature severance of the umbilical cord in assisted foalings and by hypoxia due to other causes. The foals may be normal for some hours after birth. Clinical signs include aimless wandering, apparent blindness, and convulsions including a sound like a dog barking. Called also barkers and wanderers.
neonatal mortality
death in the neonatal group.
neonatal neoplasm
occurs rarely. Lymphosarcoma, benign and malignant melanoma and myeloid leukosis are recorded. Sporadic bovine leukosis, manifested by many subcutaneous tumors, is the most common form of the disease.
neonatal ophthalmia
see ophthalmia neonatorum.
neonatal septicemia
many bacteria, which are not widely invasive in older animals, can cause septicemia in neonates because of their immunological immaturity; common examples are Escherichia coli, Listeria monocytogenes, Salmonella spp., streptococci, e.g. S. suis.
neonatal spasticity
an inherited disease of calves which are normal at birth but soon develop a susceptibility to tetanic convulsions when stimulated. See also neuraxial edema.
neonatal streptococcal infection
occurs in all species, but is especially important in piglets and foals. Bacteremia and septicemia may result in the animal's death or the development of arthritis, endocarditis, meningitis or ophthalmitis. Causative bacteria are: foals—Streptococcus zooepidemicus (S. pyogenes equi); piglets—S. suis types 1 and 2, S. equisimilis; calves—S. pyogenes; lambs—S. faecalis and group C streptococci.
neonatal thrombocytopenic purpura
a severe bleeding disease in piglets a few days old which have drunk colostrum containing antiplatelet antibody from their alloimmune dam.
neonatal vigor
amount of physical activity displayed by the newborn animal; an indication of the potential viability of the patient.