Neonatal Jaundice

Neonatal jaundice is fairly common phenomenon, which should not be automatically considered as a disease, because it is quite natural process, which is usually self-limiting and disappears without any treatment. However, its severe forms must be intensively treated as they may cause irreversible brain damage with life-long consequences.


Jaundice is caused by accumulation of a substance known as bilirubin in tissues including the skin and mucous membranes. Bilirubin is produced as a decay product of hemoglobin metabolism. Hemoglobin is present in red blood cells and it carries breathing gases. After death of a red blood cell, the hemoglobin is released and processed giving birth to bilirubin molecules. Liver tissue further processes bilirubin by so-called conjugation, which makes bilirubin water-soluble and after that, bilirubin is excreted into the bile. Increased breakdown of red blood cells may cause inadequate capacity of bilirubin processing and this can cause the jaundice (information about other mechanisms of jaundice development can be found in related article).


In case of neonatal jaundice, the main reason is the above mentioned breakdown of red blood cells. The fetal red blood cells contain a different type of hemoglobin as the erythrocytes in a newborn. In a newborn, the old erythrocytes break down and they are replaced by new ones with the new type of hemoglobin. Bilirubin is released in excessive amount and the liver of a newborn, especially in premature infants, is unable to handle the load of bilirubin contributing to its accumulation in the body.


Note: Uncommon, but a very dangerous reason for the breakdown of red blood cells in the newborn is known as the hemolytic disease of the newborn. It occurs, when the red blood cells of the child are attacked by his mother's immune organism leading to massive hemolysis.


In an embryo, bilirubin is taken away by placenta, but after the birth, this is not possible. Hemolytic disease of the newborn must be prevented, or intensively treated (see related article).


The main symptom is yellow coloration of the skin, mucous membranes and eyes of the newborn. In severe forms of diseases with high concentrations of bilirubin, its molecules may penetrate into the brain and damage it irreparably. In the acute phase, the brain damage manifests with epileptic seizures, eating disorders, unconsciousness and eventually death. Long-term consequences include irreversible brain damage associated with mental retardation, movement disorders and sensitivity disorders. Bilirubin brain damage in the newborns is technically known as kernicterus. In adults, this can not happen, because the mature brain is protected against bilirubin penetration.


The diagnosis is made by a pediatrician by a simple look. More accurate information can be obtained from a blood sample, which allows us to state the precise concentration of serum bilirubin. 


In most cases, no treatment is necessary and the key is to prevent dehydration of the child (usually by sufficient breastfeeding) and to reasonably expose the child to the sunlight, which accelerates the breakdown of bilirubin in the skin. More severe cases must undergo special phototherapy (light therapy), which means exposure of the child to a source of blue light. The blue component of the light spectrum is the most efficient in disintegration of skin and subcutaneous bilirubin. The most serious forms including hemolytic disease of the newborn require quick removal of a large amount of bilirubin. This may be ensured by exchange transfusions.


Jiri Stefanek, MD  Author of texts: Jiri Stefanek, MD
 Sources: basic text sources