Newborn jaundice


Newborn jaundice - also newbornsicterus or icterus neonatorum (old Greek icteros = jaundice) - describes the appearance of yellowing of the skin and dermis of the eyes ("Sclera") of the newborns. This yellow coloration is caused by the accumulation of breakdown products of the red blood pigment (hemoglobin). The breakdown product responsible for this is called bilirubin.
Jaundice in the first days of life is usually a physiological, harmless process that occurs in around 60% of newborns.
It is an expression of the replacement of the red blood pigment (hemoglobin) from the fetus by the adult ("adult") dye of the newborn.

Newborn jaundice that lasts more than two weeks after birth is called jaundice prolongatus.

The jaundice often reaches its full extent around the 5th day of life, after which it usually heals on its own and without consequences. Only rarely are bilirubin concentrations so high that threatening complications can occur ("Kernicterus"or"Bilirubin encephalopathy').


Newborn jaundice can have a variety of causes, but first of all you have to choose between the physiological, harmless jaundice and the jaundice due to congenital or acquired Metabolic disorders in the Bilirubin breakdown can be distinguished.
The physiological, harmless newborn jaundice is caused by an increased breakdown of the prenatal red blood pigment (fetal hemoglobin), which is replaced by adult (adult) hemoglobin after birth. By having the responsible Enzymes However, if they are immature and not fully active in the liver, the bilirubin cannot be broken down as quickly as it occurs and is deposited in the skin and the sclera.

Newborn jaundice due to disturbances in the bilirubin metabolism or an excess amount of red blood pigment apart from the normal hemoglobin change after birth can in turn have numerous causes. These include e.g. Bruisingthat occurred in newborns during childbirth and need to be removed, biliary stasis due to congenital narrowing or obstruction of the Bile duct, Inflammation of the liver (hepatitis) or a blood cell breakdown (Hemolysis) because of a Blood group intolerance between child and maternal blood group during pregnancy ("Rh factor intolerance" or. Haemolyticus neonatorum disease).
Also, prolonged neonatal jaundice can be a sign of a congenital hypothyroidism or one Neonatal infection be.


Often - depending on the severity of the jaundice - there is only a visible yellowing of the skin and the sclera of the newborn without any further symptoms. The yellow color itself cannot be felt by the offspring. This is usually the case in the context of physiological, harmless neonatal jaundice.
However, if for various reasons massive amounts of bilirubin accumulate, which cannot be broken down and excreted, this can in turn penetrate some nerve cells in the brain and lead to cell death there (Nuclear ncterus). A wide variety of symptoms, mainly neurological, can then occur.
These include a striking one Poor drinking and tiredness or indifference of the newborn, weakened newborn reflexes, high-pitched screaming, cramps in the neck and back muscles (Opisthotonus) and a downward look of the eyes when the eyelids are opened (sunset phenomenon).

Laboratory values

Newborn jaundice occurs in over 50% of all newborns in the first few weeks of life. The yellowing of the skin is often due to completely natural processes at this age. The Height of Bilirubins is a marker for the severity of newborn jaundice. The bilirubin is yellow Breakdown product of the red blood pigment hemoglobin. An increase in bilirubin above age-typical values ​​must be further clarified and treated. Heavily increased bilirubin values ​​can lead to serious damage to the newborn. The bilirubin determination can be done non-invasively through the skin. The degree of yellowness of the skin is determined via a light signal and compared with age-appropriate standard values. For a more precise assessment of increased values, the total bilirubin in the blood is usually determined.

In the first week of life, in the sense of normal (physiological) neonatal jaundice, the total bilirubin must not exceed 15 mg / dl. Everything above is pathological, so it has disease value. On the first day of life, the total bilirubin value must not exceed 7 mg / dl. If this is the case, one speaks of premature newborn jaundice (Jaundice praecox). In contrast, neonatal jaundice can be called Icterus prolongatus also last for a week. To find the cause, in addition to the total bilirubin, a further breakdown in the blood into direct and indirect bilirubin must be made.
Appropriate therapy is initiated depending on the level of the values. For babies born at the appointment, phototherapy is initiated from a value of more than 20 mg / dl. In premature babies, the indication for phototherapy is usually made earlier, as even lower values ​​lead to damage. A blood exchange transfusion must be initiated in children born at full maturity with a value above approx. 25 mg / dl.

Read about this too: Kernicterus


"Normal" neonatal jaundice, which occurs as part of the hemoglobin exchange, usually does not last longer than the 10th day of life. If jaundice persists, possible causes must be clarified.

Physiological, harmless newborn jaundice usually begins right in the first days of life (approx. 3.-6. Day), often has its climax around the 5th day of life and then develops gradually without consequences up to about the 10th day of life back.
However, if the children are already born with neonatal jaundice, or if it occurs within the first 24-36 hours, one speaks of one early Jaundice (Jaundice praecox), which is usually based on a blood group incompatibility between mother and child (Morbus haemolyticus neonatorum). Does the mother have another blood group characteristic (Rhesus factor) as the child, it can happen that the mother antibody against the “foreign” blood cells of the child and these antibodies enter the child's blood system. This can lead to a destruction of the red blood cells in the child and an increased attack of the red blood pigment. If the neonatal jaundice lasts longer than two weeks, contrary to the rule, it is referred to as prolonged jaundice (Icterus prolongus) designated. Under certain circumstances, this can be an indication of a disorder of the bilirubin metabolism, which can be congenital or acquired and requires further clarification.

Consequences / late effects

A physiological, harmless neonatal jaundice of mild to moderate intensity usually heals on its own without consequences. So there are no (late) consequences.
However, if the bilirubin concentration in the blood exceeds a certain threshold value (Icterus gravis = more than 20 mg / dl), there is a risk of bilirubin “crossing” into the brain and thus kernicterus with the destruction of nerve cells. This preferably leads to cell destruction in the so-called basal ganglia. These are brain structures that are of great importance for the regulation of movement, information and emotion processing processes.
If a newborn suffers from kernicterus, adequate therapy must be initiated as soon as possible (usually from bilirubin concentrations of> 15 mg / dl) to prevent irreversible brain damage.
Otherwise there can be serious long-term consequences for the child, caused by mental and motor development delays, epileptic seizures, movement disorders (spasticity in the context of a infantile cerebral palsy) and deafness are marked.

Is Newborn Jaundice Contagious?

The causes of physiological neonatal jaundice are not due to infection. There is therefore no risk of infection. The pathological neonatal jaundice can in rare cases be caused by a infectious hepatitis to be triggered. Infection depending on the type of hepatitis is then potentially possible.


Since physiological neonatal jaundice usually heals on its own after one to one and a half weeks without consequences, no therapy is actually necessary.
However, if the bilirubin concentration in the newborn's blood rises too high, a suitable therapy is primarily carried out to prevent the dreaded complication of kernic terus.
The two most common therapy options are phototherapy on the one hand and so-called exchange transfusion on the other.
In phototherapy, artificial light in the blue range (430-490nm wavelength) is used to irradiate the newborn. As a result, the bilirubin is converted from its previously insoluble form ("unconjugated") into a water-soluble form ("conjugated") and can thus be excreted in the bile and urine. The step is therefore taken over which the immature enzymes of the child's liver cannot cope with in full activity.
However, strict attention must be paid to adequate protection of the eyes from the radiation and adequate hydration during phototherapy, as the newborns lose fluids through increased sweating.

If the phototherapy does not produce a satisfactory result, an exchange transfusion can be tried as a further therapeutic means, especially in the context of jaundice due to blood group incompatibility between mother and child. This usually happens when the mother has a rhesus negative and the child has a rhesus positive blood group, so that the mother forms antibodies against the child's blood group characteristic, which then leads to the destruction of the child's red blood cells.
In exchange transfusions, blood is taken from the newborn via the umbilical vein and rhesus-negative blood is administered until all of the newborn's blood has been exchanged. This should prevent further breakdown of blood cells and an increase in bilirubin levels.

Homeopathy for newborn jaundice

The means used in homeopathic therapy or for the prevention of newborn jaundice include various substances: On the one hand, can phosphorus given as the main remedy.
Furthermore can China are used, a homeopathic remedy made from the bark of the Chinese tree, which is often used in cases of blood group intolerance, and Lycopodium (Pollen of the barnacle moss) and Aconite (Monkshood).