Jaundice in newborns
The content of the article:
- Causes of Jaundice in Newborns and Risk Factors
- Forms of the disease
- Symptoms of Jaundice in Newborns
- Diagnostics
- Treatment for jaundice in newborns
- Possible complications and consequences of jaundice in newborns
- Forecast
- Prevention
Jaundice in newborns is a physiological or pathological condition that is caused by an increase in the level of bilirubin in the blood and is manifested by an icteric color of the skin and mucous membranes.
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According to statistics, in the first weeks of life, jaundice develops in about 60% of cases in term babies and in 80% of cases in premature babies. Most often (60–70%) physiological jaundice is diagnosed in newborns, which occurs when the level of bilirubin in the blood rises to 70–90 µmol / L in term infants and more than 80–120 µmol / L (depending on the weight of the child) in premature babies. In most cases, jaundice manifests itself in the first three days of a child's life and does not require treatment.
Bilirubin belongs to the main bile pigments in the human body. Normally, it is formed by the breakdown of proteins (cytochrome, hemoglobin, and myoglobin) that contain heme. In the blood, bilirubin is contained in two fractions - free and bound. Approximately 96% of the bilirubin in the blood is represented by insoluble indirect bilirubin, which forms complexes with albumin. The remaining 4% bind to polar molecules, in particular to glucuronic acid. Indirect (unbound) bilirubin is formed mainly during the destruction of red blood cells and the breakdown of hemoglobin, it does not dissolve in water, dissolves in lipids and is quite toxic due to its ability to easily penetrate cells and have an adverse effect on their vital activity. Indirect bilirubin binds to blood albumin and is transported to the liver. Direct (bound) bilirubin is a low-toxic fraction of total bilirubin, which is formed in the liver. When combined with glucuronic acid, bilirubin becomes water-soluble. Most of the direct bilirubin enters the small intestine, glucuronic acid is cleaved from it, bilirubin is reduced to urobilinogen. In the small intestine, part of the urobilinogen is reabsorbed and enters the liver through the portal vein. The rest of the urobilinogen enters the large intestine, is reduced to stercobilinogen, in the lower parts of the large intestine it is oxidized to stercobilin and excreted in the feces, giving it its characteristic brown color. A small amount of stercobilinogen is absorbed into the bloodstream and then excreted in the urine.bilirubin becomes water-soluble. Most of the direct bilirubin enters the small intestine, glucuronic acid is cleaved from it, bilirubin is reduced to urobilinogen. In the small intestine, part of the urobilinogen is reabsorbed and enters the liver through the portal vein. The rest of the urobilinogen enters the large intestine, is reduced to stercobilinogen, and is oxidized to stercobilin in the lower parts of the large intestine and excreted in the feces, giving it its characteristic brown color. A small amount of stercobilinogen is absorbed into the bloodstream and then excreted in the urine.bilirubin becomes water-soluble. Most of the direct bilirubin enters the small intestine, glucuronic acid is cleaved from it, bilirubin is reduced to urobilinogen. In the small intestine, part of the urobilinogen is reabsorbed and enters the liver through the portal vein. The rest of the urobilinogen enters the large intestine, is reduced to stercobilinogen, in the lower parts of the large intestine it is oxidized to stercobilin and excreted in the feces, giving it its characteristic brown color. A small amount of stercobilinogen is absorbed into the bloodstream and then excreted in the urine. In the small intestine, part of the urobilinogen is reabsorbed and enters the liver through the portal vein. The rest of the urobilinogen enters the large intestine, is reduced to stercobilinogen, and is oxidized to stercobilin in the lower parts of the large intestine and excreted in the feces, giving it its characteristic brown color. A small amount of stercobilinogen is absorbed into the bloodstream and then excreted in the urine. In the small intestine, part of the urobilinogen is reabsorbed and enters the liver through the portal vein. The rest of the urobilinogen enters the large intestine, is reduced to stercobilinogen, in the lower parts of the large intestine it is oxidized to stercobilin and excreted in the feces, giving it its characteristic brown color. A small amount of stercobilinogen is absorbed into the bloodstream and then excreted in the urine.
The excretory function of the liver of a newborn child is significantly reduced due to anatomical immaturity and reaches the eliminating (i.e., excreting, removing) ability of the liver of an adult by the end of the first month of life.
The peculiarities of the intestinal metabolism of bile pigments in newborns determine the partial return of indirect bilirubin to the blood and an increase or persistence of an increased level of bilirubin. 80-90% of bilirubin in newborns is represented by an indirect fraction. When the enzyme systems of the body begin to function in full, the color of the child's skin returns to normal.
Causes of Jaundice in Newborns and Risk Factors
The immediate cause of jaundice in newborns is an increase in the level of bilirubin in the blood.
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Physiological jaundice can be due to the following reasons:
- rapid destruction of fetal hemoglobin;
- insufficient transfer of bilirubin across hepatocyte membranes;
- immaturity of the liver enzyme systems;
- low elimination ability of the liver.
The causes of pathological jaundice of newborns are:
- severe course of diabetes mellitus in a pregnant woman;
- Rh-conflict between mother and fetus;
- asphyxia, birth trauma;
- Gilbert's syndrome;
- diseases of the thyroid gland;
- infectious lesions of the child's liver (viral hepatitis, herpes, toxoplasmosis, cytomegalovirus, listeriosis, etc.);
- sickle cell anemia, thalassemia;
- erythrocyte membranopathy;
- cystic fibrosis;
- toxic-septic liver damage;
- violation of bilirubin excretion (bile thickening syndrome, intrauterine cholelithiasis, intestinal obstruction, pyloric stenosis, compression of the bile ducts by neoplasm or infiltration from the outside);
- the presence in breast milk of maternal estrogens, which interfere with the binding of bilirubin;
- unsteady lactation and relative malnutrition of the child;
- taking certain drugs (sulfonamides, salicylates, large doses of vitamin K).
Risk factors are too long intervals between breastfeeding, prematurity, stimulation of labor, delay in cord clamping.
Forms of the disease
Jaundice in newborns can be physiological (transient) and pathological. Pathological on the etiological basis are divided into the following types:
- conjugation - develop against the background of a violation of the processes of conversion of indirect bilirubin;
- hemolytic - due to intense hemolysis of erythrocytes;
- mechanical (obstructive) - occur when there are mechanical obstacles to the outflow of bile into the duodenum;
- hepatic (parenchymal) - develop with lesions of the liver parenchyma with hepatitis of various etiologies, hereditary metabolic disorders, sepsis.
By origin, jaundice is hereditary or acquired.
Depending on laboratory criteria, jaundice in newborns can be with a predominance of direct (more than 15% of the total) or indirect (more than 85% of the total) bilirubin.
The degree of jaundice in newborns:
| The degree of jaundice | Icteric skin | Bilirubin level μmol / l |
| I | Face, neck | > 80 |
| II | Face, neck, back, chest, belly to the navel | 150 |
| III | All skin down to the elbows and knees | 200 |
| IV | Whole body except skin on palms and soles | > 250 |
| V | Whole body | > 350 |
Symptoms of Jaundice in Newborns
Physiological jaundice in newborns occurs on the second or third day after birth and reaches a maximum on the fourth or fifth day. The skin and mucous membranes of the newborn are yellow (mild yellowness), urine and feces are of normal color, the liver and spleen are not enlarged. The yellowness of the skin does not extend below the level of the umbilical line and is noticeable only in bright natural light. The general well-being of the child usually does not deteriorate, however, in the case of a significant increase in the level of bilirubin in the blood, lethargy, lethargy, drowsiness, nausea and vomiting (regurgitation) may occur. With the organization of proper feeding and care, the symptoms of jaundice in a newborn completely disappear by about two weeks of age.
Jaundice in premature newborns, as a rule, appears earlier (the first or second days), reaches its peak by the seventh day of life and disappears by the age of three weeks. Due to the longer maturation of the liver enzyme systems in premature infants, there is a risk of developing nuclear jaundice, as well as bilirubin intoxication.
With hereditary conjugational jaundice in newborns, there is a slight increase in the level of indirect bilirubin, while anemia and splenomegaly are absent. The pathological process occurs in the first days of a child's life and is growing steadily. There is a risk of developing kernicterus with subsequent death.
Jaundice against the background of endocrine pathology manifests itself on the second or third day of a child's life and subsides by three to five months. In addition to the icteric skin, lethargy, arterial hypotension, decreased heart rate, pastiness, and constipation are noted.
The severity of jaundice that develops in a newborn against the background of asphyxia and birth trauma depends on the level of bilirubin in the blood and the severity of the hypoxic-asphyxia syndrome.
Jaundice in breastfed babies can occur in the first or second week of life and persist from one to one and a half months.
With the progression of hyperbilirubinemia in newborns, bilirubin crosses the blood-brain barrier and is deposited in the basal nuclei of the brain (kernicterus), leading to the development of bilirubin encephalopathy. At the same time, at the initial stage of the pathological process, symptoms of bilirubin intoxication (monotonous cry, apathy, drowsiness, regurgitation, vomiting) prevail in the clinical picture. Then to these symptoms are added the stiffness of the muscles of the occiput, bulging of the large fontanelle, muscle spasms, convulsions, recurrent agitation, nystagmus, bradycardia, and extinction of reflexes.
At this stage, which can last from several days to several weeks, irreversible damage to the central nervous system occurs. Over the next two to three months, children show an apparent improvement in their condition, however, already in the third or fifth month of life, such children may develop neurological complications.
Indicators of physiological and pathological jaundice:
| Index | Physiological jaundice | Pathological jaundice |
| Well-being of the child | No symptoms of illness, good appetite | The child is lethargic, does not suck well at the breast, spits up. Congenital reflexes are reduced |
| Visualization of jaundice | 2-3 days of life |
Early: congenital or onset within 24 hours after birth Late: Appears at 2 weeks of life and later |
| The degree of bilirubinemia on days 3-5 |
I – III Bilirubin <204 μmol / L |
III – V Bilirubin> 221 μmol / L |
| Jaundice | Monotonous build-up, then gradual final fade | Wave-like: it appears, then disappears and appears again |
| Duration of jaundice | The first two weeks of life | More than 2-3 weeks |
| Direct bilirubin at 2–3 weeks of life | <5.1 μmol / l | > 15-25 μmol / L |
Diagnostics
Jaundice is usually diagnosed by a neonatologist while the baby is in the hospital.
A visual assessment of the degree of jaundice in newborns is carried out according to the Kramer scale, has five degrees:
- The concentration of bilirubin is approximately 80 μmol / l, the yellowness of the skin of the face and neck.
- Bilirubin is about 150 μmol / l, yellowness extends to the navel.
- Bilirubin reaches 200 μmol / l, yellowness of the skin up to the knees.
- Bilirubin about 300 μmol / l, yellowness of the skin of the face, trunk, extremities (excluding the palms and soles).
- Bilirubin 400 μmol / l, total yellowness.
Laboratory diagnostics usually includes a complete blood count, determination of the blood group and Rh factor of the mother and child, biochemical blood test (liver function tests), general urinalysis, coagulogram, direct Coombs' test.
Determination of intrauterine infections is carried out by the methods of enzyme immunoassay, polymerase chain reaction. If hypothyroidism is suspected, laboratory determination of thyroid hormones (thyroid stimulating hormone, thyroxine, triiodothyronine) in the blood is carried out.
In addition, ultrasound of the liver and bile ducts, X-ray examination of the abdominal organs, magnetic resonance cholangiography, fibrogastroduodenoscopy may be needed.
Treatment for jaundice in newborns
Physiological jaundice in newborns does not require treatment. It is recommended to feed 8-12 times a day without a night break, the daily volume of fluid intake should be increased by 10-20% compared to the physiological need of the child.
Treatment of pathological jaundice in newborns depends on the etiological factor and is primarily aimed at eliminating it. In order to accelerate the excretion of bilirubin, enterosorbents, choleretic drugs, vitamins of group B can be prescribed. The method of phototherapy is used in an intermittent or continuous mode. In some cases, treatment for jaundice in newborns includes infusion therapy, plasmapheresis, hemosorption, replacement blood transfusion.
Possible complications and consequences of jaundice in newborns
Physiological jaundice in newborns passes without complications, however, in case of violation of adaptation mechanisms, physiological jaundice can be transformed into pathological.
The consequences of jaundice in newborns, which developed against the background of a particular pathological process, include nuclear hyperbilirubinemia with toxic brain damage, deafness, cerebral palsy, mental retardation.
Forecast
The prognosis for physiological jaundice of newborns is favorable
In the case of timely adequate treatment of pathological jaundice, the prognosis is also favorable, it worsens with the development of neurological complications.
Prevention
Specific prevention of jaundice in newborns has not been developed.
The measures for non-specific prevention of a pathological condition include:
- adequate and timely treatment of somatic diseases in a woman during pregnancy;
- giving up bad habits during pregnancy;
- rational nutrition of a pregnant woman;
- early attachment of the newborn to the breast;
- prevention of Rh-conflict.
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Anna Aksenova Medical journalist About the author
Education: 2004-2007 "First Kiev Medical College" specialty "Laboratory Diagnostics".
The information is generalized and provided for informational purposes only. At the first sign of illness, see your doctor. Self-medication is hazardous to health!
