Jaundice in Infants

Jaundice - What Does It Mean?

Jaundice is a common sign in both premature and full-term infants. The most striking feature of jaundice is the appearance of noticeable yellowish skin tones, supported by the increase in bilirubin levels in the body.

Jaundice usually first appears on the face, then spreads to the chest, abdomen, arms, and legs as bilirubin levels rise.

The whites of the eyes may also become yellowish, while for obvious reasons, jaundice may be less noticeable in dark-skinned infants.

Bilirubin is a yellow-orange pigment derived from the splenic degradation of hemoglobin contained in red blood cells, which is then made soluble by the liver to be eliminated with bile and urine. In the bloodstream, bilirubin is therefore found in two distinct forms: an indirect , not yet processed by the liver, and a direct, or conjugated, resulting from the hepatic metabolism of the previous one.

Causes

The jaundice of newborns is supported on the one hand by the increased synthesis of indirect bilirubin and on the other by the still ineffective activity of the liver enzymes intended for its metabolism.

Not surprisingly, now that the baby's lungs have begun to function and the availability of oxygen is greater than the uterine environment, many aged and supernumerary red blood cells have no reason to exist; after birth, the spleen is therefore loaded with dispose of this excess, producing large quantities of indirect bilirubin that accumulate in the tissues.

The cutaneous jaundice of the newborn, in particular, occurs when this pigment reaches and exceeds concentrations of 5/6 mg per 100 ml of blood.

Risk factors

The most common risk factors for neonatal jaundice include: prematurity, gestational diabetes, asphyxia during childbirth, hypoxia, hypoglycemia, acidosis, polycythemia, altitude, dehydration, large bruises and familiarity with jaundice (parents, brothers or sisters of the child who has had high bilirubin levels in the past, requiring treatment with phototherapy).

Normal or Pathology?

Newborn jaundice is an extremely common condition, affecting more than 50% of healthy full-term newborns. Physiological jaundice appears around the second day of life, peaks on the third or fourth day and then it begins to regress until it disappears within a week or two. As mentioned in the introductory part, physiological neonatal jaundice is characterized by indirect hyperbilirubinemia, while jaundice episodes accompanied by high levels of conjugated bilirubin are considered abnormal.

The conditions for which neonatal onset jaundice is considered pathological are the following:

appearance in the first 24 hours;
daily increase in blood bilirubin greater than 5 mg / dL;
total bilirubin values greater than 13 mg / dL in the term newborn and 15 mg / dL in the preterm infant;
direct bilirubin concentration above 1.5-2 mg / dL;
association of morbid conditions that aggravate the potential risk (severe prematurity, very low birth weight, asphyxia and other risk factors);
persistence of jaundice and hyperbilirubinemia beyond one week in the full-term infant and beyond two weeks in the preterm infant.

Symptoms not to be underestimated, which require a quick medical consultation, are represented by: marked yellow color of the skin also at the level of the abdomen, arms and legs; yellowish coloring of the ocular sclera (the white part of the eye); irritability, deep sleep, refusal to breastfeed or bottle-feed.

Causes of Pathological Jaundice

The causes of pathological jaundice are many and can be distinguished in hemolytic forms, characterized by indirect hyperbilirubinemia, and cholestatic forms or by reduced hepatic uptake and / or conjugation of the hepatic pigment, characterized by direct hyperbilirubinemia. The first group includes the most common cause of neonatal jaundice. : it is called haemolytic disease due to maternal-fetal incompatibility and is due to the passage, through the placenta during pregnancy or during labor, of maternal antibodies against antigens present on fetal red blood cells; the most severe form generally occurs starting from the second pregnancy in Rh-positive infants with inadequately treated Rh-negative mothers.

Another common cause of jaundice is linked to neonatal anemias, characterized by a reduced survival of the red blood cells and an increased catabolism of the abnormal forms. Even infections or poisoning of various types and the intake of certain drugs or toxic substances are typically accompanied by jaundice from increased hemolysis. Metabolic diseases (Gilbert's syndrome, galactosemia, Crigler Najjar syndrome, Lucey-Driscoll syndrome) and hypothyroidism are instead responsible for the jaundice forms due to reduced uptake and / or hepatic conjugation of bilirubin.

Phototherapy is also used to treat cases of neonatal jaundice.

It is useful thanks to the consequent isomerization of bilirubin which is thus transformed into compounds that the newborn can excrete in the urine or feces. Typically the so-called bili light therapy is used (420-470 nm)

The potential damage due to hyperbilirubinemia occurs above 20 mg / dl, due to the possibility that the pigment crosses the blood-brain barrier, depositing itself in the nerve cells.

Complications and Treatment

Where required, bilirubin levels can be lowered by irradiating the child with special light sources (phototherapy); alternatively or in association with this intervention, the intravenous injection of albumin can avoid the deposition of the pigment in the tissues, while waiting to be adequately disposed of by the liver. Phenobarbital also represents a therapeutic aid commonly used in episodes of neonatal jaundice with indirect hyperbilirubinemia .