See also: yellow eyes
Jaundice: What does it mean?
Jaundice is a sign of common confirmation in both premature and full-term infants. The most striking feature of jaundice is the appearance of evident yellowish skin nuances, sustained by the increase in bilirubin levels in the body.
Usually jaundice appears first on the face, then spread to the chest, abdomen, arms and legs as bilirubin levels increase.
Bilirubin is a yellow-orange pigment derived from the splenic degradation of hemoglobin contained in red blood cells, then made soluble by the liver to be eliminated with bile and urine. In the blood circulation, bilirubin is therefore found in two distinct forms: an indirect one, not yet processed by the liver, and a direct, or conjugate, deriving 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 liver enzymes intended for its metabolism.
Not by chance, now that the child's lungs have begun to function and the availability of oxygen is greater than in the uterine environment, many aged and supernumerary red blood cells have no reason to exist; after birth, the spleen then takes care of disposing of this excess, producing large quantities of indirect bilirubin that accumulate in the tissues.
The newborn's cutaneous jaundice, in particular, occurs when this pigment reaches and exceeds concentrations of 5/6 mg on 100 ml of blood.
Risk factors
Among the most common risk factors for neonatal jaundice are: prematurity, gestational diabetes, asphyxia during childbirth, hypoxia, hypoglycemia, acidosis, polycythemia, altitude, dehydration, large bruising and familiarity for jaundice (parents, brothers or sisters) of the child who had elevated bilirubin levels in the past, such as to require phototherapy treatment).
Normality or Pathology?
Newborn jaundice is an extremely widespread condition, affecting more than 50% of healthy newborns at term of pregnancy. The physiological jaundice appears approximately towards the second day of life, reaches its peak during the third or fourth day and then begins to regress until it vanishes within a week or two. As stated in the introductory part, physiological neonatal jaundice is characterized by indirect hyperbilirubinemia, while jaundice episodes accompanied by elevated 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 bilirubinemia greater than 5 mg / dL;
- total bilirubin values greater than 13 mg / dL in the term newborn and 15 mg / dL in preterm;
- direct bilirubin concentration above 1.5-2 mg / dL;
- association of morbid conditions that aggravate its potential risk (severe prematurity, very low birth weight, asphyxia and other risk factors);
- persistence of jaundice and hyperbilirubinemia over a week in the term newborn and over two weeks in preterm.
Symptoms to be reckoned with, which require a rapid medical consultation, are represented by: marked yellow skin color also in the abdomen, arms and legs; yellowish coloring of the ocular sclerae (the white part of the eye); irritability, deep sleep, refusal to breastfeed or artificial.
Causes of Pathological Jaundice
The causes of pathological jaundice are multiple and distinguishable in hemoltic forms, characterized by indirect hyperbilirubinemia, and cholestatic forms or reduced pigment hepatic uptake and / or conjugation, characterized by direct hyperbilirubinemia. The first group includes the most common cause of neonatal jaundice: it is called hemolytic 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 usually occurs starting from the second pregnancy in Rh positive infants with inadequately treated Rh negative mothers.
Another common cause of jaundice is related to neonatal anemias, characterized by a reduced survival of the red blood cells and an increased catabolism of the anomalous forms. Even infections or intoxications of various types and the intake of certain drugs or toxic substances are typically accompanied by jaundice with increased haemolysis. Metabolic diseases (Gilbert's syndrome, galactosemia, Crigler Najjar syndrome, Lucey-Driscoll syndrome) and hypothyroidism are instead responsible for the icteric forms due to reduced uptake and / or hepatic conjugation of bilirubin.
Phototherapy is also used to treat cases of neonatal jaundice.
it is useful for the consequent isomerization of bilirubin which is thus transformed into compounds that the newborn can expel with urine or faeces. The so-called light therapy (420-470 nm) is typically used
The potential damage due to hyperbilirubinemia takes place above 20 mg / dl, due to the possibility that the pigment exceeds the blood-brain barrier by depositing in 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, intravenous albumin injection can prevent the deposition of pigment in the tissues, while waiting to be properly disposed of by the liver. Phenobarbital is also a therapeutic aid commonly used in episodes of neonatal jaundice with indirect hyperbilirubinemia.
