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Jaundice in newborns is a physiological or pathological condition that occurs in the first week of life with hyperbilirubinemia and skin discoloration and visible yellowing of the mucous membranes.
Jaundice in infants is associated with elevated bilirubin levels in the blood, anemia, yellowing of the skin, mucous membranes and sclera, hepatosplenomegaly, and, in severe cases, bilirubinemic encephalopathy.
The Kramer scale is used in the diagnosis of infantile jaundice, in addition to the amount of erythrocytes, bilirubin, liver enzymes, maternal and child blood group. Treatment of jaundice includes breastfeeding, infusion therapy, phytotherapy, and blood transfusions.
Infantile jaundice is a process characterized by neonatal syndrome, yellowing of the skin and visible mucous membranes. Neonatal jaundice occurs in 60% of premature infants and 80% of premature infants. In the field of pediatrics, 60-70% of all cases of jaundice are due to physiological processes. Jaundice occurs when the level of bilirubin in the blood exceeds 80-90 μmol / l (in premature infants) and 120 μmol / l (in premature infants). Prolonged and severe jaundice is toxic to the brain and damages nerve cells.
Classification and causes of jaundice in infants
First of all, it is important to know that jaundice in newborns can be physiological or pathological death. Hereditary or acquired jaundice can be differentiated by origin. There are also types of jaundice caused by an increase in bound bilirubin and unbound bilirubin on blood biochemical tests.
First of all, it is important to know that jaundice in newborns can be physiological or pathological death. hereditary or acquired jaundice differs in origin. There are also types of jaundice caused by an increase in bound bilirubin and unbound bilirubin on blood biochemical tests.
Conjugated jaundice includes the following cases:
- Neonatal physiological (transient) jaundice;
- Hereditary jaundice in Gilbert, Kriegler-Nayara type I and II syndromes;
- Jaundice due to asphyxia and birth trauma;
- Jaundice caused by various drugs (salicylates, chloramphenicol, sulfonamides, quinines, large amounts of vitamin K);
- Hemolytic jaundice occurs in infants as a result of the breakdown of erythrocytes (hemolysis). Such hyperbilirubinemia includes:
- Hemolytic disease of the fetus;
- Erythrocyte enzymes and membranopathies;
- Hemoglobinopathies (sickle cell anemia, thalassemia);
- Polycythemia.
Mechanical jaundice is caused by impaired secretion of bilirubin from the bile or intestines. It occurs as a result of atresia and hypoplasia of the intrahepatic and extrahepatic bile ducts, fetal gallstone disease, tumor or infiltrate obstruction of the bile ducts, bile thickening, pylorostenosis, intestinal obstruction, and others.
Mixed jaundice (parenchymatosis) in infants, fetal hepatitis, intrauterine infection (toxoplasmosis, cytomegalovirus, listeriosis, herpes, hepatitis A, B, D), toxic-septic liver damage, hereditary diseases (cystic fibrosis, galactosemia).
Signs of jaundice in infants
Physiological jaundice in infants
Transient jaundice is a transient physiological condition in newborns. As soon as the baby is born, fetal hemoglobin begins to break down and the amount of free bilirubin in the blood increases.
Incomplete enzymes in the liver (glucuronyltrasferase) and strong reabsorption of bound bilirubin in the intestines also cause jaundice. Physiological jaundice develops within 2-3 days after birth and reaches its maximum in 4-5 days. The amount of unbound bilirubin is 77-12 μmol / l. Breath and urine are normal in color, and the spleen is not enlarged.
At the slight level of transient jaundice, the skin color drops to the navel. During physiological jaundice, the baby's general condition does not change, but when hyperbilirubinemia is severe, the child may experience symptoms such as drowsiness, weakness, and nausea.
In children, physiological jaundice is normal and disappears spontaneously by 2 weeks. In premature infants, jaundice appears earlier, ie 1-2 days after birth, reaches a maximum at 7 days and passes in 3-4 weeks.
The amount of unbound bilirubin in the blood exceeds 137-171 μmol / l. Premature infants are more likely to develop bilirubin intoxication and nuclear jaundice because liver enzymes are also unable to function properly.
Hereditary jaundice
Hereditary jaundice is the most common constitutional hyperbilirubinemia (Gilbert's syndrome), occurring in 2-6% of the population, and is inherited in an autosomal dominant type. Gilbert's syndrome disrupts the activity of the liver enzyme hyuronyltransferase, which prevents hepatocytes from binding bilirubin.
In hereditary jaundice, Kriegler-Nayar syndrome, there is a decrease in the activity of the enzyme glucuronyltransferase (type I) or no enzyme at all (type II). Type I jaundice occurs in the first days of a child's life and gradually worsens, with hyperbilirubinemia in the blood up to 428 μmol / l or even higher.
The development of nuclear jaundice as a result of the disease can be fatal. Type II is of good quality. Hyperbilirubinemia occurs in the blood at a level of 257-376 μmol / l. Nuclear jaundice rarely develops.
Jaundice that develops due to endocrine pathologies
It is most common in children born with congenital hypothyroidism, thyroid deficiency, incomplete formation of liver enzymes, impaired bilirubin conjugation and excretion. Hypothyroidism In 50-70% of children, jaundice occurs in 2-3 days of life and persists for 3-5 months. In addition to jaundice, such children may experience weakness, adynamism, arterial hypotension, bradycardia, constipation such as
In addition, children born to mothers with diabetes are more likely to develop jaundice due to hypoglycemia and acidosis. It has a high content of unbound bilirubin.
Jaundice in newborns: as a result of asphyxia and birth trauma
Fetal hypoxia and neonatal asphyxia delay the development of the enzymatic system, resulting in hyperbilirubinemia and nuclear jaundice. Various birth traumas (cephalohematoma, ventricular hemorrhage) cause an increase in unbound bilirubin levels and severe jaundice.
Aries syndrome or jaundice occurs in 1-2% of children who are fed naturally. It can appear in the first week of life (early jaundice) or 1-7 weeks (late jaundice), which lasts for 14-4 weeks. The pathophysiology of this syndrome is explained by the presence of estrogen hormones in breast milk, and in breastfed infants, the bilirubin metabolism is disturbed by the action of hormones.
Risk factors for the development of jaundice in naturally fed infants include late meconium separation, late umbilical cord miscarriage, and artificial stimulation of labor. The consequence of such jaundice is positive in any situation.
Nuclear jaundice and bilirubin encephalopathy
As the amount of unbound bilirubin continues to increase, it slowly crosses the hematoencephalitic barrier and damages the basal nuclei of brain cells, leading to a dangerous condition called bilirubin encephalopathy.
Symptoms of bilirubin intoxication in the clinic of the disease are: fatigue, apathy, drowsiness, monotonous crying, vomiting. Typical symptoms of nuclear jaundice are: stiffness of the neck muscles, muscle spasms, intermittent agitation, elevated larynx, reflex disorders, nystagmus, bradycardia, convulsions such as. This pathological condition lasts from a few days to a few weeks, during which time there is irreversible damage to the central nervous system. The child's condition improves after 2-3 months, but this is a "lie", and by 3-5 months the child begins to develop neurological complications: BSF (DSP), ZPR, deafness and others.
Diagnosis of jaundice in infants
Jaundice is diagnosed by a neonatologist or pediatrician in the maternity ward as soon as the baby is born. The Kramer scale is used to assess the degree of jaundice:
- Grade I - jaundice on the face and neck (bilirubin 80 μmol / l);
- Grade II - jaundice spreads to the umbilicus (bilirubin 150 μmol / l);
- Grade III - jaundice spreads to the knee (bilirubin 200 μmol / l);
- Grade IV - jaundice spreads to face, torso, arms and legs (300 μmol / l);
- Grade V is jaundice throughout the body (bilirubin level 300 μmol / l).
In the detection of jaundice in infants, general blood tests, blood biochemical tests, maternal and child blood group, Coombs' test, PTI, general urine analysis, liver tests are performed. When hypothyroidism is suspected, the amount of thyroid hormones T3, T4, TTG is checked. Intrauterine infection is detected using IFA and PSR tests. In order to detect mechanical jaundice, tests such as liver UTT, MR-cholangiography, FGDS, abdominal X-ray are performed. A pediatric surgeon and gastroenterologist are also required.
Treatment of jaundice in infants
To reduce jaundice and eliminate hyperbilirubinemia, each child should be breastfed, preferably at least 8-12 times a day.
Children are increased daily fluid intake by 10-20% and enterosorbents are prescribed. If oral hydration is not possible: infusion therapy - glucose, saline, ascorbic acid, cocarboxylase, B and C vitamins are given intravenously. Phenobarbital can be used to stimulate bilirubin binding.
The most effective way to treat unrelated hyperbilirubinemia is phototherapy. In this case, unbound bilirubin appears to be water-soluble.
Hemolytic jaundice is treated with blood transfusions, hemosorption, and plasmapheresis. All neonatal jaundice requires treatment of the underlying disease.
Consequences and prevention of infantile jaundice
Transient jaundice in infants is usually uncomplicated. However, as a result of disruption of the adaptation mechanism, the physiological condition can become pathological. Children with pathological jaundice are examined and registered by a local pediatrician and pediatric neurologist.