Breast milk jaundice in newborns Komarovsky. Jaundice in newborns: when should pass, Dr. Komarovsky

Physiological jaundice is the normal state of a newborn during the period of adaptation to new environmental conditions. Staining of the skin and eye sclera in yellow is caused by the accumulation in the blood of a coloring pigment - bilirubin. The baby’s liver and kidneys are not able to immediately remove all excess bilirubin from the body, so this condition is considered the norm and is not a reason for treatment.

But this applies only to physiological jaundice. If the pathology is caused by diseases of the liver, bile ducts or gall bladder, the child needs urgent medical attention. For example, with biliary atresia of the biliary tract, an infant needs Kasai surgery, which must be performed before the child reaches the age of three months. So that in case of deviations, the baby can get the necessary help on time, parents need to know when physiological jaundice in the newborn should pass.

During intrauterine development, certain types of proteins accumulate in the child’s blood: hemoglobin, myoglobin and cytochrome. Their structure is different from adult blood proteins. During the passage of the baby through the birth canal and within a few hours after birth, the hemoglobin decomposes and is replaced by other types of proteins that have different properties and functions.

During the breakdown of hemoglobin, bilirubin, the main component of bile, which functions as a coloring pigment, is released. The organ that processes bilirubin and is responsible for its removal from the body is the liver. In a newly born baby, the liver is not able to produce the necessary amount of enzymes that destroy bilirubin, so it begins to accumulate in the body and cause characteristic symptoms: yellowing of the eye sclera and skin integument.

Note! If a woman has hormonal problems associated with increased synthesis of steroid hormones belonging to the estrogen group, the probability of developing jaundice in a child will be more than 85%. The fact is that estriol and estradiol are able to accumulate in breast milk and enter the body of the baby, who will get rid of them in the first place. Thus, excess bilirubin will linger in the blood, and jaundice will last several times longer compared to infants whose mothers did not suffer from endocrine disorders.

How long does it take?

Yellowing of the skin in most children occurs on the third day of life - it is during this period that the replacement of blood proteins and the release of bilirubin ends. A nurse in the postpartum ward every day measures the level of bilirubin using a special photo device that is applied to the frontal part. A slight excess of the norm is considered permissible, but the child is taken under special control.

On 3-4 days after birth, signs of jaundice can be seen without any devices. The skin of the child acquires a bright yellow color, sclera turns yellow, yellowing of the nail plates may be noted (the child’s nails are thin, and through them you can see the yellow skin under the nails). In the case of pathological jaundice, the baby's skin may acquire an unnatural lemon tint. At the same time, the following symptoms can be observed in the child:

• frequent, restless crying;
• poor appetite;
• weight loss significantly higher than normal;
• inhibition of reactions and weakness of congenital reflexes;
• constant drowsiness with short periods of sleep (the newborn often wakes up and screams without opening his eyes);
• mismatch of the size of the abdomen with physiological norms and the weight with which the child was born.

If jaundice has physiological causes, it goes away on the 5-7th day of a child’s life. During this time, the child will receive therapy using special photolamps. Healthy children are usually discharged from the maternity hospital on day 5. If the yellowness of the skin does not pass by this time, mother and baby can be left in the hospital for a period of 7-10 days. This period is considered optimal for eliminating physiological yellowing.

Important! In some maternity hospitals with a small number of free places, one mother can be discharged and the child left for aftercare for another 3-5 days. Of course, a woman has the right to pick up a child and refuse treatment, provided that she will undergo the necessary procedures at the place of residence, but doctors do not advise doing this. In the presence of pathologies of the liver and gall bladder, timely diagnosis is very important, therefore it is better to leave the baby under the supervision of specialists (if the attending physician insists on this), who can provide the necessary assistance in case of emergency.

The child is discharged with jaundice

The situation when a baby is discharged from the hospital with signs of jaundice is quite common. There is nothing wrong with this, since in some cases yellowness of the skin can persist for up to 3 weeks. Of great importance is the observance by a woman of a diet for nursing mothers (it is necessary to exclude any products containing a large number of coloring pigments), as well as the implementation of all the doctor's recommendations. The child may be prescribed physiotherapeutic treatment, which the mother can take in the clinic at the place of residence, but pediatricians do not approve of this approach because of the high risk of infection of the child.

If the mother notices that the yellowness of the child does not go away, but the baby is being prepared for discharge, you should not worry. Before discharge, such a child must carry out:

• biochemical blood and urine tests;
• ultrasound examination of the liver, gall bladder and bile ducts;
• liver tests - a blood test that helps to compile a clinical picture of the state of the liver and evaluate the functioning of liver enzymes.

Indicators of ALT (liver function tests) in children of the first year of life

A doctor observing a child must evaluate the dynamics of changes in the level of bilirubin in the blood and draw a conclusion about the nature of jaundice. If the child does not show signs of a pathological course, he will be discharged from a medical institution, and his mother will be given recommendations on the regimen, care and treatment (if necessary).

Jaundice appeared after discharge from the hospital

If jaundice first appears after the baby has been discharged from the maternity ward, this can be an alarming sign. There may be several reasons for this condition:

• hormonal problems in women who breastfeed;
• endocrine disorders in the body of the baby;
• errors in the diet for nursing mothers;
• impaired metabolism;
• viral infections (e.g., hepatitis).

In some cases, late jaundice can be associated with a Rh conflict of the mother and fetus, as well as a mismatch in the blood group (very rare). Regardless of what reason caused the appearance of such symptoms, the child needs to be shown to the doctor and a blood test taken. If necessary, the doctor will prescribe an ultrasound and other diagnostic measures to accurately determine the cause of the pathology.

The baby went the second month, but jaundice does not go away

If the baby is already 1 month old and the skin still retains a yellowish tint, an examination will be required. In exceptional cases, the physiological jaundice can last up to 3 months, but the pathological nature must be excluded.

In most cases, jaundice in infants older than 1 month indicates serious diseases that require examination and treatment in a hospital. It is possible that the child will need surgical treatment.

Such diseases include:

• biliary atresia (obstruction of the biliary tract);
• cirrhosis of the liver;
• mechanical damage to the liver or bile ducts;
• gallbladder disease;
• stagnation of bile and bile acids.

Important! All these diseases have a high mortality rate in infancy, therefore, it is impossible to ignore the symptoms of pathological jaundice. If, after 3-4 weeks after birth, the signs of jaundice in the baby do not disappear, you must go to the hospital.

Video: What if jaundice persists?

How to determine that the jaundice disappears?

The first sign indicating the recovery of the child is the gradual disappearance of the yellow tint. First of all, the mucous membranes of the organs of vision usually turn pale, then the skin of the abdomen and limbs. The longest signs of yellowness can persist on the face, but they do not completely disappear 2-3 days after the appearance of positive dynamics.

The child's well-being is also improving. The baby becomes more active, his periods of wakefulness increase, his sleep becomes longer and calmer. Behavioral changes also become noticeable. The child becomes calmer, bouts of sudden crying appear less often. If you carefully observe the baby, you will notice that he is trying to fix his gaze on objects and begins to respond to the voice of his mother or another person who is caring for him.

All these symptoms together indicate that the blood counts are returning to normal, the level of bilirubin is reduced, and the work of the liver and gall bladder corresponds to physiological norms.

Is treatment required?

Most of the babies have jaundice and pass on their own on the 7-10th day of life (maximum 3-4 weeks). Medication is usually not prescribed, but if the amount of bilirubin in the blood significantly exceeds the permissible norms, the child is shown phototherapy sessions. The baby is placed under a special ultraviolet lamp, covering the eye area with protective glasses. The duration of the procedure is determined individually, as well as the duration of treatment.

At home, the child is recommended to sunbathe. In summer they can be done throughout the day, but it is better to choose periods when the sun is not particularly active: morning (before 11-12 hours of the day) or evening (after 16-17 hours). In winter, on the contrary, it is better to arrange baths in the interval from 13 to 16 hours, since this time ultraviolet rays are most active and penetrate well through the atmospheric layer. The procedure is performed as follows:

• the baby must be completely undressed (including the diaper);
• on a hard surface, on which sunlight falls, lay a thick diaper (it is better to use a flannel);
• put the baby on a diaper and leave it for 10-12 minutes, periodically turning it from the tummy to the back and back.

During the procedure, it is necessary to distract the child, tell tales or sing songs. He still does not understand the meaning of the words spoken, but he perfectly captures the intonations of a familiar voice that will help him calm down. If the baby continues to cry, you can stroke it or pick it up, going to the window.

Important! Parents must ensure that there are no drafts in the place where the child is. It is also worth remembering that sunbathing is contraindicated if the child has a fever.

If a viral infection has become the cause of jaundice, a course of antiviral drugs, as well as enzymes that restore liver cells and improve the functioning of the organ, can be prescribed. In case of blood diseases, iron preparations can be used, as well as cytostatic (antitumor) drugs - their choice and the need for taking depends on which disease caused the accumulation of bilirubin.

Jaundice is a physiological condition of a newborn baby, which in most cases does not require medical treatment. Normally, jaundice passes on the 10th day of the baby’s life, but protracted forms also occur (up to 3-4 weeks). If the skin retains a yellowish tint, and the child is already a month old, you must go to the hospital - the cause may be severe pathologies of the liver and biliary tract, requiring emergency surgical care. read on our website. learn by reference.

Video - Jaundice

Video - Jaundice of the newborn

A sharp yellowing of the skin in a baby on 3-5 days of life is a common phenomenon. More than half of all newborns experience this physiological symptom. Mom should not be scared, because this is a natural process of development of the body of crumbs. It is enough to wait a few days when the jaundice in the newborn should pass. At the same time, do not leave the child unattended so as not to miss a possible pathology.

The famous doctor Yevgeny Komarovsky repeatedly reassured in his speeches parents worried about when the jaundice should pass in newborns. As the doctor explains, the characteristic symptoms are manifested due to the normal process of adaptation of the baby to new living conditions.

While the baby developed in the mother’s stomach, oxygen entered his body through the placenta. Therefore, another type of hemoglobin was used for its transportation. After birth, substances that become unnecessary are destroyed, and the composition of the blood changes to the standard for each person.

Jaundice in newborns

When destroying unused cells, bilirubin is released. It is this substance that paints the skin yellow. Usually it is processed by liver enzymes, and then excreted in the urine, staining it in the usual shades. Jaundice in an adult is a symptom of a dangerous pathology, signaling that the organs do not function as they should. But in a newborn everything is different.

The body of crumbs in the first days of life at an accelerated pace gets used to the new conditions of life and nutrition. The child’s liver does not yet know how to work at full strength, not having time to process all the bilirubin that is released during the natural replacement of blood. But after a few days, the body accumulates a sufficient amount of enzymes, and the jaundice passes by itself.

How to speed up the process

According to Dr. Komarovsky, normal treatment is not required, and it’s enough to wait until she needs to go through herself. Mom should not particularly worry about this. But if you want to help the baby's body, then you can use simple tips:

1. Milk. Breastfeeding slows the initial processing of bilirubin, prolonging jaundice. This is due to the composition of the mother’s milk. But at the same time, it is the enzymes that are contained in it that accelerate the normalization of the liver. If you do not stop breastfeeding, the baby will return to its usual color much faster. Therefore, it is important to ensure that the crumbs do not forget to eat regularly due to the concomitant jaundice of drowsiness.
2. Walks. No pills and medications are needed to treat jaundice. Destroy bilirubin helps ordinary sunlight. Therefore, the baby should be regularly taken for walks. If the weather permits, it is advisable to spend as much time as possible in the fresh air.
3. Lamp. If the weather on the street is inclement, then you should not catch a baby in danger. At home, you can help the baby's body if he sleeps under a lamp. Blue spectrum light works best. But in the absence of special devices, any bright lighting is enough. Just do not forget to protect the baby’s eyes by putting on a bandage or hat.

Normally, the moment when the jaundice in newborns should pass under the lamp occurs at the end of the first week of life. Without extra effort, just wait a couple more days. Thus ends the natural stage of liver development.

When to sound an alarm

There are conditions when the lemon color of the skin and mucous membranes is not a sign of normal development of the liver, but a signal of serious violations in the work of the body of the crumbs. In this case, it is important to pay attention to the symptoms on time, especially if the mother decided not to visit the hospital:

1. Time. Normally, jaundice develops only 3-5 days after birth. Pathological conditions manifest themselves almost immediately. It is also worth paying the attention of a specialist to the health of the child if the skin has not regained its standard color even by the third week of life.
2. Urine and feces. With natural jaundice, the bowel movements of the baby retain their natural shades. But with violations in the body, urine becomes much darker. Feces, on the contrary, are discolored.
3. Behavior. Normally, despite the lemon shade of the skin, the baby will behave as usual. Unless it will become a little longer. But with pathologies of the internal organs, anxiety of the crumbs will be noticeable. A nervous child will lose her appetite, will be lethargic.
4. Analyzes. A doctor, taking the blood of a newborn for examination, can immediately say whether there are violations in the natural development. Normally, the level of hemoglobin in the crumbs does not fall. The body gradually replaces some cells with others, while maintaining a natural concentration of substances in the blood. But with pathology, anemia will be immediately noticeable due to the mass death of red blood cells.
5. Inspection. With pathology, the doctor will also be able to identify malfunctions in the body of the crumbs without laboratory tests. The baby will increase the liver and spleen. Also, there will be noticeable expansion of the veins on the anterior abdominal wall. Bruises can spontaneously appear on the skin.

The body of each child is unique. Only a specialist can accurately say when the jaundice in a newborn should go, and how to treat a possible pathology. To maintain the health of the crumbs, you should not try to do something yourself without prior consultation.

Causes and consequences of pathologies

Malfunctions in the work of the body of a newborn can be caused by many reasons. Some are harmless enough. Others may even require surgery:

Given the variety of possible causes of the development of pathological jaundice, treatment methods in individual situations differ. But most often, mom should not worry too much. At this age, most of the pathologies can be corrected, providing the possibility of further normal development of the crumbs.

Treatment methods and consequences of jaundice

Bilirubin itself can be toxic if the body does not cope with the excretion of its decay products. Prolonged jaundice can lead to a pathological change in blood composition. This, in turn, will affect the development of all organ systems. But the nervous system will suffer the most.

With physiological jaundice, such problems do not arise. But the pathological condition is dangerous, even if you do not take into account additional risk factors from the causes that caused a change in the color of the skin and mucous membranes.

Therefore, in addition to treating the causes of the problem, the doctor will definitely prescribe therapy to remove bilirubin from the body of the crumbs:

1. Blue lamp. Phototherapy in a hospital is carried out by light radiation with a wavelength of 450 nm. The child is prescribed to be under the lamp for 12-14 hours. It is absolutely safe, but it helps turn toxic bilirubin breakdown products into safe chemicals.
2. Medicines Doctors can administer medications to help the baby's body process bilirubin. Typically, hepatoprotectors, choleretic drugs and vitamin complexes are used for these purposes. In severe cases, detoxification is carried out using a dropper containing pure saline or glucose.
3. Blood transfusion. If other methods do not have the desired effect, the doctor may prescribe a transfusion. This is an extreme measure, because the child’s body can react negatively to the procedure with a severe allergic reaction. There is also always the risk of incorrect procedure, which leads to an air embolism or infection in the bloodstream. But still, if the doctor insists on a transfusion, mother should not refuse, because this is an attempt to save the life of a child in a crisis situation.

Most often, after overcoming the difficult period of the first stages of development of the baby, other problems should not be expected. The child will grow up healthy and cheerful if the mother timely draws the attention of specialists to a possible problem.

Jaundice, or a visual manifestation of hyperbilirubinemia, includes syndromes of various origins, a common feature of which is icteric staining of the skin and mucous membranes. In total, there are about 50 diseases that are accompanied by the appearance of yellowness of the skin. In adults, skin staining occurs with an increase in bilirubin level of more than 34 μmol / l, in newborns - with a level of bilirubin from 70 to 120 μmol / l.

Jaundice of the neonatal period, due to the accumulation of excess bilirubin in the blood, is common and sometimes requires urgent medical measures. Indirect bilirubin is a neurotoxic poison and under certain conditions (prematurity, hypoxia, hypoglycemia, prolonged exposure, etc.) causes a specific lesion of the subcortical nuclei and cerebral cortex - the so-called bilirubin encephalopathy. According to various sources, in the first week of life, jaundice occurs in 25-50% of full-term and 70-90% of premature infants.

Bilirubin is the final product of heme catabolism and is formed mainly due to the breakdown of hemoglobin (about 75%) with the participation of hemoxygenase, biliverdin reductase, as well as non-enzymatic reducing substances in the cells of the reticuloendothelial system (RES). Other sources of bilirubin are myoglobin and heme-containing liver enzymes (about 25%).

The natural isomer of bilirubin - indirect free bilirubin - is soluble in lipids, but poorly soluble in water. In the blood, it easily enters into a chemical bond with albumin, forming a bilirubin-albumin complex, due to which only less than 1% of the resulting bilirubin enters the tissue. Theoretically, one molecule of albumin can bind two molecules of bilirubin. In combination with albumin, bilirubin enters the liver, where it penetrates the cytoplasm by active transport, binds to Y and Z proteins, and is transported to the endoplasmic reticulum. There, under the influence of uridine diphosphate glucuronyl transferase (UDFGT), bilirubin molecules combine with glucuronic acid and monoglucuronide birirubin (MHB) is formed. When MGB is transported through the cytoplasmic membrane to the bile capillaries, the second bilirubin molecule joins and diglucuronide birirubin (DHB) is formed. Conjugated bilirubin is water-soluble, non-toxic and excreted in the bile and urine. Next, bilirubin in the form of DHB is excreted into the bile capillaries and excreted along with bile into the intestinal lumen. In the intestine, under the influence of intestinal microflora, a further transformation of bilirubin molecules occurs, as a result of which stercobilin is excreted with feces.

Almost all stages of bilirubin metabolism in newborns are characterized by a number of features: a relatively larger amount of hemoglobin per unit of body weight, moderate hemolysis of red blood cells even under normal conditions, even in a healthy full-term newborn baby, the content of Y- and Z-proteins, as well as the activity of UFHT are sharply reduced in the first day of life and make up 5% of the activity of such systems in adults. An increase in the concentration of bilirubin leads to an increase in the activity of liver enzyme systems within 3-4 days of life. Complete formation of liver enzyme systems occurs by 1.5-3.5 months of life. Morphofunctional immaturity, endocrine disorders (hypothyroidism, increased progesterone in human milk), disorders of carbohydrate metabolism (hypoglycemia), the presence of concomitant infectious pathology significantly extend the formation of liver enzyme systems. The processes of excretion of bilirubin from the body are also imperfect, which is associated with increased intestinal reabsorption of bilirubin. The population of the intestines of a newborn with normal intestinal microflora dramatically reduces the amount of bilirubin absorbed from the intestine, and helps to normalize the processes of its excretion from the body.

All jaundice is usually divided by the level of the bilirubin metabolism block:

• on suprahepatic (hemolytic), associated with increased decay of red blood cells, when liver cells are not able to utilize the avalanche-forming large amounts of bilirubin;
• hepatic (parenchymal), associated with the presence of an inflammatory process that disrupts the function of liver cells;
• subhepatic (mechanical) associated with a violation of the outflow of bile.

In the practice of a neonatologist, a pathogenetic classification of jaundice of newborns is used (according to N.P. Shabalov, 1996), according to which there are:

• Jaundice caused by increased production of bilirubin (hemolytic): hemolytic disease of the newborn, polycythemic syndrome, swallowed blood syndrome, hemorrhage, drug hemolysis (overdose of vitamin K, oxytocin, the use of sulfonamides, etc.), hereditary forms of erythrocytic membranes and fermentopathies, hemoglobin.
• Jaundice due to reduced clearance of bilirubin by hepatocytes (conjugation): hereditary syndromes of Gilbert, Krigler-Nayyar type I and II, Arias, metabolic disorders (galactosemia, fructosemia, tyrosinosis, hypermethioninemia, etc.), impaired conjugation of high bilirubinorrhea with pil obstruction, the use of certain drugs.
• Jaundice due to impaired evacuation of conjugated bilirubin with bile through the bile ducts and intestines (mechanical): anomalies in the development of bile ducts in combination with other malformations (Edwards syndrome, Aladzhill syndrome), family cholestasis of Bayler, McElfresh, Rotor and Dubin-Johnson syndromes, cystic fibrosis, -1-antitrypsin deficiency, bile condensation syndrome, compression of the biliary tract by a tumor, infiltrates, etc.
• Mixed genesis: sepsis, intrauterine infections.

The following signs always indicate the pathological nature of jaundice: the appearance of jaundice on the first day of life, a bilirubin level of more than 220 μmol / l, an hourly increase in bilirubin of more than 5 μmol / l per hour (more than 85 μmol / l per day), its duration is more than 14 days, wave-like course of the disease, the appearance of jaundice after the 14th day of life.

Most common cause conjugation hyperbilirubinemia in newborns, there is a mismatch between the normal production of bilirubin and the imperfect system of its removal from the body due to the immaturity of the liver enzyme systems. Conjugation jaundice is characterized by its appearance on the 3rd day of life, the absence of an increase in the liver and spleen, changes in the color of the stool and urine, anemic symptom complex.

For transient hyperbilirubinemia of the newborn jaundice is characteristic at the age of more than 36 hours of life. The hourly increase in bilirubin should not exceed 3.4 μmol / l h (85.5 μmol per day). The highest intensity of icteric staining of the skin occurs on the 3-4th day, while the maximum level of bilirubin does not rise above 204 μmol / L. Transient hyperbilirubinemia is characterized by a progressive decrease in bilirubin level and intensity of jaundice after 4 days and its extinction by the 8-10th day. The general condition of the child is not violated. No treatment required.

For jaundice premature infants an earlier onset is characteristic (1-2 days of life), which creates difficulties in differentiating it with hemolytic disease of the newborn. However, anamnesis (blood type of mother and child, lack of sensitization) and laboratory tests (normal levels of hemoglobin, red blood cells, lack of reticulocytosis) help to make a correct diagnosis. The duration of conjugation jaundice in premature infants is up to 3 weeks.

In 1963, I. M. Arias described mother's jaundice”(Pregnan jaundice) in breast-fed infants. The pathogenesis of this type of jaundice is not fully understood. However, it is believed that its cause is the low conjugation of bilirubin, which is a consequence of the inhibitory effect of pregnanediol, which is found in excess in the blood of some women in the postpartum period, as well as reduced excretion of bilirubin. The duration of jaundice is from 3 to 6 weeks. The diagnostic test is the abolition of breastfeeding on the 2-3rd day, against which jaundice begins to resolve quickly. With the resumption of breastfeeding, the bilirubin level begins to rise again.

Gilbert's syndrome (constitutional hepatic dysfunction) - an inherited disease inherited in an autosomal dominant manner. The frequency in the population is 2-6%. The reason is a hereditary violation of conjugation of indirect bilirubin due to impaired capture of the latter by the liver cell. In newborns, the disease resembles transient jaundice. Cases of nuclear jaundice are not described. The forecast is favorable. The diagnosis is made on the basis of a family history of persisting hyperbilirubinemia in the absence of other pathological changes. The appointment of phenobarbital leads to a sharp decrease in jaundice, which also indicates the presence of this disease.

The inherited pigment exchange disorder in Kriegler-Nayyar syndrome is due to the absence (type I) or very low activity (type II) of glucuronyl transferase in the liver cells.

With Krigler-Nayyar syndrome Type I disease is inherited in an autosomal recessive manner. Intense jaundice is characteristic from the first days of life with an increase in the level of indirect serum bilirubin 15-50 times higher than normal, with a complete absence of a direct fraction of bilirubin. In the natural course of the disease, in most cases, the nuclei of the brain are stained, and a fatal outcome can be noted. Phenobarbital administration is ineffective. The only treatment is phototherapy and liver transplantation.

In type II disease, which is inherited in an autosomal dominant type, along with less intense jaundice and the level of indirect bilirubin is 15-20 times higher than normal, a direct fraction of bilirubin is determined in the blood. A distinctive feature is a positive response to the appointment of phenobarbital. Predictably, Kriegler-Nayyar type II syndrome is more favorable. The development of bilirubin encephalopathy is extremely rare.

The first symptom of hereditary metabolic disorders, such as galactosemia, fructosemia, tyrosinemia and others, there may also be jaundice, which is conjugative in nature. First of all, the doctor should be wary of a combination of prolonged jaundice with symptoms such as vomiting, diarrhea, hepatomegaly, progressive hypotrophy, severe neurological symptoms in the form of seizures, muscle hypotension, paresis, paralysis, ataxia, cataracts, and mental retardation. The diagnosis is confirmed by the presence of galactose in the urine, positive samples for sugar and other special methods for detecting metabolic disorders in each individual case.

Jaundice in hypothyroidism it is observed in newborns depending on the degree of insufficiency of the thyroid gland function and is combined with other symptoms of the disease, such as large birth weight, severe edematous syndrome, low timbre of the newborn’s voice, early and persistent constipation, etc. In the biochemical analysis of blood along with indirect hyperbilirubinemia there is an increase in cholesterol. The screening test for hypothyroidism is positive, the level of thyroid stimulating hormone in the blood is increased with a decrease in T4. Prolonged (from 3 to 12 weeks) jaundice with hypothyroidism is due to a slowdown in all metabolic processes, including the maturation of glucuronyltransferase systems of the liver. Timely diagnosis (during the first month of life) and the appointment of thyroidin or L-thyroxine replacement therapy lead to the normalization of bilirubin metabolism.

Jaundice with polycythemia (diabetic fetopathy) due to a delay in the maturation of enzyme systems of the liver on the background of hypoglycemia with increased hemolysis. Monitoring and correction of hypoglycemia, the appointment of inducers of microsomal liver enzymes contribute to the normalization of bilirubin metabolism.

Jaundice with pyloric stenosis and high intestinal obstruction due to a violation of the conjugating systems of the liver due to dehydration and hypoglycemia, and increased reverse absorption of bilirubin from the intestine. In this situation, only the elimination of pyloric stenosis and intestinal obstruction lead to the normalization of pigment metabolism.

The use of drugs (glucocorticoids, some types of antibiotics, etc.) can lead to a sharp disruption of the conjugation processes in the liver due to the competitive type of metabolism of the above drugs. In each case, an analysis of therapeutic measures is required, as well as knowledge of the metabolic characteristics of the drugs prescribed for the newborn.

All hemolytic jaundices are characterized by the presence of a symptom complex, including jaundice on a pale background (lemon jaundice), an increase in the liver and spleen, an increase in the level of indirect bilirubin in the blood serum, and normochromic anemia with reticulocytosis of varying severity. The severity of the condition of the child is always due not only to bilirubin intoxication, but also the severity of anemia.

Hemolytic disease of the newborn arises as a result of incompatibility of the blood of the mother and the child according to the Rh factor, its subtypes or blood groups. The disease proceeds in the form of edematous, icteric and anemic forms. The edematous form is the most severe and is manifested by a congenital anasarca, severe anemia, hepatosplenomegaly. As a rule, such children are not viable. The icteric and anemic forms of the disease are more favorable, but can also pose a threat to the health of the child. In mild cases, the level of hemoglobin in cord blood is more than 140 g / l, the level of indirect bilirubin in the blood serum is less than 60 μmol / l. In this case, conservative therapy is sufficient. With hemolytic disease of newborns of moderate severity and severe course, a replacement blood transfusion operation may be required. In the clinical picture, jaundice is either congenital or appears during the first days of life, has a pale yellow (lemon) tint, is steadily progressing, against the background of which neurological symptoms of bilirubin intoxication may appear. Hepatosplenomegaly is always noted. Changes in the color of feces and urine are uncharacteristic.

Damage to the structures of the central nervous system (CNS) occurs with an increase in the level of indirect bilirubin in the blood serum of full-term newborns above 342 μmol / L.

For premature babies, this level ranges from 220 to 270 μmol / L, for deeply premature babies - from 170 to 205 μmol / L. However, it must be remembered that the depth of the central nervous system lesion depends not only on the level of indirect bilirubin, but also on the time of exposure in the brain tissue and associated pathology that aggravates the child’s serious condition.

Preventive measures to prevent the development of hemolytic disease of newborns, which should be carried out already in the antenatal clinic, are to register all women with a Rh-negative and with 0 (I) blood type, to clarify the history of the sensitization factor, to determine the level of Rh antibodies and, if necessary, early delivery. All women with Rh-negative blood on the first day after birth are shown the introduction of anti-D-globulin.

With the development of hemolytic disease, a newborn is given a replacement blood transfusion; in the preoperative period, photo and infusion therapy is used.

Hereditary hemolytic anemia are very diverse. The most common of these is Minkowski-Shoffar microspherocytic hemolytic anemia. The defective gene is localized in the 8th pair of chromosomes. The result of the mutation is the production of abnormal red blood cells having a spherical shape and smaller (less than 7 nm) sizes that undergo excessive destruction in the crypts of the spleen. The anamnesis is characterized by the presence in the family of relatives with a similar disease. The diagnosis is confirmed by the detection of microspherocytic red blood cells, a shift of the Price-Jones curve to the left, a decrease in the osmotic resistance of red blood cells, a change in the sphericity index and the average concentration of hemoglobin in red blood cells. The disease proceeds in waves, hemolytic crises accompanied by fever, decreased appetite and vomiting. Crises are triggered, as a rule, by acute viral diseases, hypothermia, the appointment of sulfonamides, etc. Splenectomy is considered the main treatment method.

During the neonatal period, another type of hereditary hemolytic anemia can be detected, characterized by a change in the shape of red blood cells - the so-called infantile pycnocytosis. The first signs of the disease appear in the first week of life and more often in premature babies. Red blood cells in a stained blood smear have spine-shaped processes. In addition to anemia, edema and thrombocytosis are also detected. The appointment of vitamin E at a dose of 10 mg / kg per day leads in most cases to clinical and laboratory remission.

When examining a blood smear in newborns, target erythrocytes can also be detected, which is typical for hemoglobinopathies (thalassemia, sickle cell anemia). Sickle cell anemia is more common among residents of Central Asia, Azerbaijan and Armenia and is manifested in the neonatal period only in homozygous carriers of s-hemoglobin.

Diagnosis hereditary enzyme-penic anemia (deficiency of glucose-6-phosphate dehydrogenase, pyruvate kinase, hexogenase, 2,3-diphosphoglycerometase, phosphohexisomerase) is extremely rare for newborns, as it requires highly differentiated studies. In the clinical picture, newborns with this pathology show hemolytic anemia with reticulocytosis, an enlarged liver and spleen. A family history is characteristic.

Large hematomas in the neonatal period can also cause severe indirect hyperbilirubinemia and anemia. The presence in a child of a large size with a kefalogemate, intraventricular hemorrhages, subcapsular hematomas of parenchymal organs, massive hemorrhages in soft tissues is accompanied by a characteristic clinical picture.

Mechanical jaundice is characterized by the accumulation of direct (bound) bilirubin in the blood, which is accompanied by jaundice, which has a greenish tint, an increase in liver size, discoloration of the stool (discoloration) and urine (increase in color intensity).

The syndrome of thickening of bile in newborns develops as a complication of hemolytic disease of newborns with extensive cephalohematomas, as well as undergoing asphyxiation in childbirth. At the same time, an increase in the intensity of jaundice is noted from the end of the first week of life, accompanied by an increase in the size of the liver, sometimes significant, and partial discoloration of the stool. Treatment consists in the use of choleretics and cholekinetics.

In addition, bile thickening syndrome may be one of the earliest clinical manifestations of cystic fibrosis, especially if it is combined with meconial ileus or damage to the bronchopulmonary system. The correct diagnosis in this case is facilitated by the determination of albumin in meconium, an ultrasound scan (ultrasound) of the pancreas, and a sweat test.

Malocclusion in the neonatal period can be caused by malformations of the biliary tract: intrahepatic and extrahepatic atresia of the bile ducts, polycystosis, torsions and excesses of the gallbladder, arterihepatic dysplasia, Aladjill syndrome, syndromic decrease in the number of interlobular bile ducts.

With atresia of the biliary tract, the first sign of a malformation is jaundice, which is stubbornly growing in nature, accompanied by itching of the skin, which is why children are very restless and irritable. The size and density of the liver gradually increase, the nature of the stool changes: it becomes partially or completely discolored. The phenomena of cholestasis lead to malabsorption of fats and fat-soluble vitamins, hypotrophy and hypovitaminosis increase. At the age of 4-6 months, signs of portal hypertension and hemorrhagic syndrome appear. Without surgery, such patients die before the age of 1-2 years of life. A biochemical blood test reveals the presence of hypoproteinemia, hypoalbuminemia, an increase in direct bilirubin, alkaline phosphatase.

With tubular bile duct hypoplasia syndrome (Aladzhill syndrome), inherited in an autosomal recessive manner, other malformations are also determined: hypoplasia or stenosis of the pulmonary artery, anomalies of the vertebral arches, and kidneys. The stigmas of dysembryogenesis are characteristic: hypertelorism, protruding forehead, deep-set eyes, micrognathia.

Familial forms of cholestasis are known, manifested in the neonatal period. With McElfresche syndrome, the presence of discolored stool is noted for a long period of time, up to several months. In the future, deviations in the condition of the child are not noted. In Byler’s syndrome, on the contrary, biliary cirrhosis develops after an cholestasis episode in the first months of life.

Mechanical jaundice can be caused by compression of the bile ducts from the outside by a tumor, infiltrates and other abdominal formations. Obstruction of the common bile duct in congenital gallstone disease is often noted.

A group of hereditarily determined excretion defects of bound bilirubin is distinguished. These include Dubin-Johnson syndrome, caused by the "breakdown" of the canalicular transport system. The syndrome is inherited in an autosomal recessive manner, accompanied by a moderate increase in direct bilirubin, a slight increase in liver size, and massive excretion of coproporphyrins in the urine. In biopsy specimens in the liver cells, a brown-black pigment resembling melanin is deposited. Rotor syndrome is also inherited in an autosomal recessive manner, but this syndrome is based on a defect in the capture and accumulation of organic anions by the liver cells. The clinical picture is similar to that of Dubin-Johnson syndrome. No pigment deposits in liver cells.

The diagnosis of cholestasis syndrome during the neonatal period is made by ultrasound of the liver, radioisotope scanning, percutaneous liver biopsy, cholangiography, etc.

Parenchymal jaundice caused by damage to the liver parenchyma of an inflammatory nature. The cause of the lesion can be viruses, bacteria and protozoa: hepatitis B and C virus, cytomegalovirus, Coxsackie, rubella, Epstein-Barr, herpes simplex virus, pale treponema, toxoplasma, etc. The septic process in a newborn can be accompanied by direct bacterial liver damage.

The clinical picture of parenchymal jaundice includes a number of general and strictly specific signs: children are often born premature or immature, with intrauterine growth retardation, unweighted by gestational age, have signs of damage to several organs and systems, as a result of which their condition at birth is regarded as extremely serious. Jaundice is already present at birth and has a grayish, “dirty” shade, against the background of severe microcirculation disorders, often with manifestations of skin hemorrhagic syndrome. Hepatosplenomegaly is characteristic. In the study of biochemical analysis of blood serum, both direct and indirect fractions of bilirubin, increased activity (10-100 times) of liver transaminases, an increase in alkaline phosphatase, glutamate dehydrogenase are detected. The Eberlein method indicates serious violations in the conjugation mechanisms of the liver cell - the vast majority of direct bilirubin is represented by the fraction of monoglucuronide bilirubin. A complete blood count often reveals anemia, reticulocytosis, thrombocytopenia, leukocytosis or leukopenia. In the coagulogram, there is a deficiency of the plasma link of hemostasis, fibrinogen. To identify the causative agent of the infectious process, it is identified by polymerase chain reaction (PCR), determination of the titers of specific immunoglobulin M and immunoglobulin G. The treatment consists in the appointment of specific antibacterial, antiviral and immunocorrective therapy.

Summarizing the foregoing, we note that diagnostic measures for neonatal jaundice must take into account a number of provisions.

• When collecting an anamnesis, it is necessary to pay attention to the possible family nature of the disease: cases of prolonged jaundice, anemia, splenectomy in parents or relatives matter.
• An anamnesis on the part of the mother must necessarily contain information about the blood group and Rh factor of her and the father of the child, the presence of previous pregnancies and childbirth, operations, injuries, blood transfusions without taking into account the Rh factor. In a woman during pregnancy, a violation of glucose tolerance, diabetes mellitus, an infectious process can be detected. It is also necessary to find out if a woman has taken drugs that affect bilirubin metabolism.
• The history of the newborn includes determining the gestational age, weight and height indicators, Apgar score at birth, clarifying the nature of feeding (artificial or natural), the time of appearance of icteric staining of the skin.
• A physical examination helps determine the shade of jaundice, establish an indicative level of bilirubin using an ikterometer. The presence of a cephalogemate or extensive ecchymoses, hemorrhagic manifestations, edematous syndrome, hepatosplenomegaly is determined. You should pay attention to the nature of the color of urine and stool. An important diagnostic point is the correct interpretation of the neurological status of the child.
• Laboratory methods include a clinical blood test with the determination of hematocrit, a smear of peripheral blood (necessary for the diagnosis of disorders in the shape and size of red blood cells), determination of blood type and Rh factor in the mother and child (allows you to determine the cause of hemolytic disease of the newborn).

In addition, conducting a direct and indirect Coombs test will suggest whether there is an incompatibility of the blood of the mother and the child for rare factors.

A biochemical blood test (determination of total bilirubin and its fractions, the level of liver transaminases, alkaline phosphatase, the concentration of total protein, albumin, glucose, urea and creatinine, cholesterol and triglycerides, C-reactive protein, thymol test, etc.) allows not only diagnose the type of jaundice, but also collect data on the condition of other organs and systems that are of great importance when prescribing radical methods of treatment (for example, it is very important to have an idea of \u200b\u200bthe initial kidney function before a replacement blood transfusion, since one of the complications of this operation is acute renal failure).

The Eberlein method (determination of direct bilirubin fractions - mono- and diglucuronide bilirubin) is important in the differential diagnosis of mechanical and parenchymal jaundice.

It is also necessary to conduct tests to detect an infectious agent in the blood, stage of the disease (PCR, enzyme-linked immunosorbent assay, determination of the number and type of immunoglobulins, determination of avidity and affinity of antibodies, Wasserman reaction, etc.).

The determination of the thyroid hormone profile is performed if hypothyroidism is suspected.

The osmotic resistance of red blood cells, hemoglobin electrophoresis, screening tests for the determination of glucose-6-phosphate dehydrogenase are carried out in order to clarify the causes of hereditary hemolytic anemia.

A sweat test for suspected cystic fibrosis is performed in children older than 1 month of life; in the early neonatal period, the determination of albumin in meconium can be practiced.

Tests also include the determination of serum a-1 antitrypsin, ultrasound of the brain, and internal organs of the abdominal cavity.

X-ray method, computed tomography are performed with suspected intestinal obstruction, intracranial hemorrhage, fibroesophagogastroduodenoscopy - with suspected pyloric stenosis. A percutaneous liver biopsy is performed in controversial cases in order to verify the diagnosis.

Before starting treatment, it is necessary to determine the method of feeding the newborn: breastfeeding is not allowed with hemolytic disease of the newborn, galactosemia, tyrosinemia.

Treatment of hyperbilirubinemia

Consider the basic methods of treating hyperbilirubinemia.

• Phototherapy at the present stage is the most effective treatment for indirect hyperbilirubinemia. The essence of the action of phototherapy is the photoisomerization of indirect bilirubin, i.e., turning it into a water-soluble form. Currently, there are several varieties of blue light lamps with a wavelength of 410-460 nm, allowing you to select the desired treatment regimen (continuous, intermittent). Modern fiber-optic devices of Biliblanket are devoid of almost all side effects, are compact, do not violate the usual mode of the child and his communication with his mother. Phototherapy is started when there is a threat of bilirubin growth to a toxic value. The lamps are placed at a distance of 20-40 cm from the skin level of the child, the radiation power should be at least 5-9 nW / cm 2 / nm. Phototherapy is carried out continuously, it can be interrupted only at the time of feeding and visits of the mother. The eyes and external genitalia of the baby are covered with opaque cloth. If phototherapy is used in a newborn with direct hyperbilirubinemia, you can observe a change in the color of the skin - a “bronze baby” syndrome. Complications of phototherapy include skin burns, lactose intolerance, hemolysis, dehydration, hyperthermia, and tanning. When conducting phototherapy, measures are required to maintain a constant water balance of the newborn.
• Infusion therapy is used to prevent water balance disturbances during phototherapy using lamps with undifferentiated light; while the physiological need for fluid increases by 0.5-1.0 ml / kg / h. The basis of infusion therapy are glucose solutions, to which membrane stabilizers are added (in order to reduce peroxidation processes), electrolytes, soda (if necessary, their correction), cardiotrophics and drugs that improve microcirculation. To accelerate the excretion of bilirubin from the body, the method of forced diuresis is sometimes used. It is possible to introduce albumin solutions at a dose of 1 g / kg per day into the infusion therapy regimen.
• The feasibility of using inducers of microsomal liver enzymes (phenobarbital, zixorin, benzonal) is explained by the ability of the latter to increase the ligandin content in the liver cells and the activity of glucuronyl transferase. These inductors are used in violation of conjugation processes. Phenobarbital is used at a dose of 5 mg / kg per day, the course of treatment should not exceed 4-6 days. A phenobarbital application scheme is possible, in which high loading doses are used - 20-30 mg / kg on the first day, then 5 mg / kg on the next, but high doses of phenobarbital have a strong sedative effect and can cause respiratory failure, apnea in the newborn.
• Enterosorbents (smecta, polyphepan, enterosgel, cholestyramine, agar-agar, etc.) are included in therapy with the goal of interrupting the hepatic-intestinal circulation of bilirubin. However, they do not significantly affect serum bilirubin levels. Nevertheless, given the absence of toxic effects of these drugs, they can be used in the treatment of hyperbilirubinemia, but only as an auxiliary method.
• Synthetic metalloporphyrins have previously been widely used in the treatment of indirect hyperbilirubinemia. Their mechanism of action is based on competitive inhibition of hemoxygenase, leading to a decrease in bilirubin production. Currently, these drugs are not used in the treatment of neonatal jaundice, since the phototoxic effect of tin-protoporphyrin IX was noted.
• Replaced blood transfusion is carried out with the ineffectiveness of conservative methods of therapy, a progressive increase in the level of bilirubin, in the presence of absolute indications, that is, when there is a threat of nuclear jaundice. Replaced blood transfusion is performed in the volume of two volumes of circulating blood, which allows you to replace up to 85% of circulating red blood cells and reduce the level of bilirubin by 2 times. Indications for this procedure at present are: edematous-anemic form of hemolytic disease of the newborn, when transfusion is carried out in the first 2 hours of life; the level of indirect umbilical cord blood bilirubin is above 60 μmol / l; umbilical cord hemoglobin level below 140 g / l; hourly growth of bilirubin above 6 μmol / l; hourly growth of bilirubin above 8.5 μmol / l with a drop in hemoglobin below 130 g / l; the presence of progressive anemia; the excess of bilirubin in the next day above 340 μmol / L.
• Of choleretics and cholekinetics, in cases of cholestasis (with the exception of atresia of the extrahepatic bile ducts and impaired synthesis of bile acids due to fermentopathy), magnesium sulfate and allochol can be used, however, at present, the preference is given to the preparation of ursodeoxycholic acid - ursofalk, which is available in suspension, is lightweight dosing for newborns, characterized by a quick and distinct therapeutic effect. The initial therapeutic dose is 15-20 mg / kg per day. With insufficient effectiveness, the dose can be increased to 30-40 mg / kg per day. When carrying out long-term treatment, a maintenance dose of 10 mg / kg per day is used.
• Correction of fat-soluble vitamins is carried out with hypoplasia and atresia of the biliary tract and long-existing cholestasis in the preoperative period. Vitamin D 3 - 30 000 IU intramuscularly 1 time per month or 5000-8000 IU inside daily. Vitamin A - 25 000-50 000 IU intramuscularly 1 time per month or 5000-20000 IU inside 1 time per day. Vitamin E - 10 mg / kg intramuscularly; 25 IU / kg per day orally 1 time in 2 weeks. Vitamin K - 1 mg / kg once every 1-2 weeks.
• Correction of trace elements: calcium - 50 mg / kg per day inside, phosphorus - 25 mg / kg per day inside, zinc sulfate - 1 mg / kg inside per day.
• An increase in protein and caloric load in such children is necessary to ensure normal growth and development, in addition, medium chain triglycerides should be present in the diet. The need for such newborns in proteins is 2.5-3 g / kg, fats - 8 g / kg, carbohydrates - 15-20 g / kg, calories - 150 kcal / kg (60% - carbohydrates, 40% - fats).
• With Aladjill syndrome, non-syndromic form of intrahepatic bile duct hypoplasia, perinatal sclerosing cholangitis, etiopathogenetic treatment methods are absent. The formation of cirrhosis of the liver during these processes serves as an indication for liver transplantation.
• Extrahepatic causes of the development of cholestasis syndrome are an indication for the removal of the cause of cholestasis or surgery on Kasai, with the subsequent prevention of the development of infectious processes and sclerotic changes in the bile ducts. Anti-inflammatory therapy includes the administration of high doses of prednisone intravenously during the first week after surgery (10\u003e 2 mg / kg per day), then 2 mg / kg / day orally for 1-3 months.
• With hyperbilirubinemia caused by metabolic disorders, they most often resort to conservative methods of treatment. With galactosemia, a diet that does not contain galactose and lactose is used. In the first year of life, therapeutic mixtures are used: NAN lactose-free, Nutramigen, Prehistimil and other mixtures that do not contain lactose. With tyrosinemia, a diet is prescribed that does not contain tyrosine, methionine and phenylalanil (lofenolac, XP Analog, XP Analog LCP, Apenilac, Phenyl-Free, Tetrafen 40, etc.). in recent years, an inhibitor of the enzyme 4-hydroxyphenylpyruvate dioxygenase - nitisinone, which is prescribed at the rate of 1 mg / kg / day, orally. With fructosemia, foods containing fructose, sucrose and maltose must be excluded from the diet. Prescribed drugs that compensate for the lack of bile acids - cholic and deoxycholic at the rate of 10 mg / kg / day.
• When replacement enzyme therapy is most often used, 10,000 creon, the dose of the drug is selected according to pancreatic insufficiency, pancreatin - 1000 units of lipase / kg / day.

Literature

1. Abramchenko V. V., Shabalov N. P. Clinical perinatology. Petrozavodsk: LLC "Publishing House Intel Tech", 2004. 424 p.
2. Diseases of the fetus and newborn, congenital metabolic disorders / ed. R.E. Berman, V.K. Vaughan. M .: Medicine, 1991.572 s.
3. Degtyarev D. N., Ivanova A. V., Sigova Yu. A. Krigler-Nayyar syndrome // Russian Bulletin of Perinatology and Pediatrics. 1998. No. 4. P. 44-48.
4. Komarov F. I., Korovkin B. F., Menshikov V. V. Biochemical studies in the clinic. M .: APP "Dzhangar", 2001.
5. Neonatology / ed. T. L. Gomella, M. D. Cannigam. M.: Medicine, 1998.640 s.
6. Papayan A. V., Zhukova L. Yu. Anemia in children. St. Petersburg: Peter, 2001.
7. Guidelines for pharmacotherapy in pediatrics and pediatric surgery. Neonatology / ed. A. D. Tsaregorodtseva, V. A. Tabolin. M .: Medpraktika-M, 2003.
8. Tabolin V. A. Bilirubin metabolism in newborns. M .: Medicine, 1967.
9. Shabalov N. P. Neonatology: a manual for doctors. SPb., 1996.Vol. 1, 2.
10. Sherlock S., Dooley D. Diseases of the liver and biliary tract: a practical guide / ed. Z. G. Aprosina, N. A. Mukhina: trans. from English M .: GEOTAR Medicine, 1999.864 s.
11. Podymova S. D. Diseases of the liver. M., Medicine. 1993.
12. Balistreri W. F. Nontransplant options for the treatment of metabolic liver disease: saving livers while saving lives // Hepatology. 1994; 9: 782-787.
13. Bernard O. Early diagnosis of neonatal cholestatic jaundice // Arch. Pediatr. 1998; 5: 1031-1035.
14. Nedim Hadzie, Giorgina Mieli-Vergani. Chronic liver disease in childhood. Int. Semin. Paediatr. Gastroenterol. Nutr. 1998; 7: 1-9.

L. A. Anastasevich, Candidate of Medical Sciences
L.V. Simonova, Candidate of Medical Sciences
Russian State Medical University, Moscow

Often, newly mummified mothers, examining their newborn treasure, even in the maternity hospital notice the unusual yellowness of his skin. A children's doctor draws attention to this.Newborn jaundice makes a young mother worry. Is it worth the alarm? Where does yellowness come from? Why do babies turn yellow? Is it necessary to treat and how?

Even in the hospital, the mother may notice the yellowness of the skin of the child and begin to worry. In most cases, baby jaundice does not bode well - this is a common physiological symptom

Types of Jaundice in Newborns

Jaundice in a newborn is a fairly common occurrence. It is caused by an increased content of bilirubin in the blood and skin of the baby. Bilirubin is a reddish-yellow pigment that forms during the breakdown of hemoglobin. If it is deposited in excess in the tissues of the child, then the skin and mucous membranes of the baby acquire a typical yellow color.

First of all, mothers should know that newborn jaundice is of 2 types: physiological and pathological. Let's try to find out about each type of jaundice as much as possible.

Signs of physiological jaundice

The skin of the baby is stained 2-3 days after birth. Such a jaundice in a newborn does not go beyond the norm and usually disappears without a trace after a few days. In some children, the icteric skin color is barely noticeable, in others it is quite pronounced. The degree of manifestation of jaundice depends on the rate of bilirubin formation, as well as the ability of a small organism to excrete it. This type of jaundice also includes the so-called "jaundice of breastfeeding." The general well-being of the child in this case does not suffer, urine and feces retain their natural color, the liver and spleen do not increase.

You need to know that normally the skin acquires its natural color in the third week in full-term babies and after 4 weeks in premature babies, this is the main sign of a physiological phenomenon. This condition occurs in children without medical intervention and does not have any harmful consequences for the baby's body. Yellowness should begin to decrease already at the beginning of the 2nd week of life. Normally, physiological jaundice lasts no longer than 3 weeks and completely passes by the end of the 1st month of a child’s life.

Attention: if the yellowness of the skin of the child lasts a month or longer, the feces are colorless, the urine is dark, but the level of bilirubin does not exceed 115 μmol / l - this is not physiological jaundice. Most likely, there is a congenital pathology of the biliary tract. This condition of the child requires a thorough examination to make the correct diagnosis.

Pathological jaundice: how to quickly recognize the danger?

This type of jaundice requires close attention of mother and doctors. The norm of bilirubin in the blood of such children is greatly exceeded, and since the pigment is toxic, a gradual poisoning of the body occurs (for more details, see:). You should be wary if your baby has the following symptoms from the first days:

• dark urine and feces to an unnatural color;
• jaundice appears already in the first day of life;
• the baby is lethargic, inactive, poorly sucks;
• high levels of bilirubin in the blood;
• yellowness of the skin lasts longer than 3 weeks;
• enlarged spleen and liver (we recommend reading:);
• the child often spits up;
• pathological yawning.

Then the classic manifestations of the so-called "nuclear" jaundice appear:

• increased muscle tone;
• protrusion of a large fontanel (more in the article:);
• convulsive twitching;
• the baby screams monotonously;
• rolling eyes
• respiratory failure until it stops.

After a few days, the symptoms of jaundice decrease, but it’s too early to rejoice: later terrible signs of cerebral palsy, hearing impairment, and mental retardation develop. Pathological jaundice should be treated immediately in a specialized hospital.

Remember: the main symptom of this pathology is the early stage of its manifestation! The baby's skin becomes bright yellow almost immediately after birth.

Fortunately, the pathological form of jaundice is rare. Such jaundice is diagnosed only in 5 newborns out of 100. Parents should carefully monitor the condition of their baby in the first days of his life, so as not to be late with treatment.

Why does physiological jaundice occur?

During intrauterine life, red blood cells (red blood cells) provided oxygen to the baby's tissues, but after birth, the baby breathes on its own and now the red blood cells with hemoglobin are no longer needed. They are destroyed and in the process of their destruction, bilirubin is produced, which stains the skin of the newborn in yellow (we recommend reading:). Bilirubin is excreted in the feces and urine.

The baby’s body is only learning to function properly and is not yet able to fully cope with all its responsibilities. Jaundice in a newborn is a natural phenomenon that occurs as a result of insufficient functioning of the liver. Since the newborn’s liver is still immature, in the first days of his life, she does not have time to process all of the resulting bilirubin, so the pigment partially enters the bloodstream. It stains the mucous membranes and skin yellow. When the child’s liver grows a little, it will more carefully process the bilirubin entering it. As a rule, the liver begins to work fully by the 5th-6th day of the baby’s life. From this moment, physiological jaundice gradually fades away and there is no reason for concern.

In some children, the adjustment of liver functions is faster, in others it is slower. What determines the rate of excretion of bilirubin? A child has every chance to stay “yellow-skinned” for a couple of weeks if:

• mom is too young and has the highest bilirubin level;
• diabetes in mom;
• he was born together with a twin brother or sister;
• he was born prematurely - the liver of a premature baby is even more immature than that of babies born on time;
• mother experienced iodine deficiency during pregnancy;
• the mother did not eat well, smoked or was sick while she was carrying the baby;
• took some medications.

In some cases, the birth of twins can cause jaundice: the liver of children is rather weak, since the mother’s body resources were spent on two fruits at once

Where does pathological jaundice come from?

Most often, this formidable phenomenon happens for the following reasons:

1. Incompatibility of maternal and fetal blood by Rh factor (hemolytic disease of the newborn). Currently, it is extremely rare, since all women with a negative Rhesus receive special preventive treatment from the 28th week of pregnancy.
2. Congenital diseases or underdevelopment of the baby’s liver.
3. Genetic or hereditary abnormalities.
4. Congenital pathologies of the circulatory system or intestines of the newborn.
5. Incorrect antibiotic therapy.
6. Severe pregnancy of the mother, toxicosis, threat of termination.
7. Mechanical violation of the outflow of bile: blockage of the bile duct by a tumor, narrowing of the bile duct or their underdevelopment.

The norm of bilirubin for a newborn

How much bilirubin is in the blood is determined by a biochemical analysis. If the bilirubin level is above 58 μmol / L, then noticeable yellowness of the skin appears. With physiological jaundice, it is never higher than 204 μmol / L.

If the level of bilirubin in the blood of a full-term baby of the first three weeks of life is higher than 255 μmol / l, and premature - 170 μmol / l, then this indicates a serious pathology and requires urgent examination and treatment. He must be prescribed by a doctor.

The upper limits of the normal content of bilirubin in the blood of an infant can be found in the table:

If the yellowness of the baby’s skin against the background of breastfeeding does not go away even in the third week after birth, then doctors are talking about “jaundice of breast milk”. It is believed that the presence of mother's milk in the baby's body increases the content of bilirubin in his liver. In this case, the flowering of the jaundice falls on 11-23 days of life. This condition is very slow, in many of these babies, yellowness finally disappears by the third month, only sometimes by the second. In such cases, a thorough examination of the child is recommended to identify more serious causes of jaundice.

There is an opinion that, during breastfeeding, the level of bilirubin rises. For this reason, breastfeeding ceases when a child shows signs of jaundice, however, modern studies have confirmed the fact that breastfeeding is an important measure in the treatment of newborn jaundice. Most of the yellow pigment is excreted from the body of the baby with feces. Breast milk has a mild laxative effect, which helps to eliminate bilirubin and prevents the development of jaundice.

Indeed, an icteric shade of the skin often manifests itself in infants who are breastfeeding. However, breast milk has a high likelihood of developing jaundice in those babies who began to breastfeed late or too rarely and too little, due to a lack of milk in the mother.

Slight yellowness of the skin of the baby during breastfeeding should not bother parents, but you still need to consult a doctor

There is no evidence that breast milk jaundice does any harm to the baby. If a child who receives only breastfeeding has a light icteric skin tone, then this is not scary and should not disturb parents.

Jaundice treatment

Treatment of a pathological process that can cause serious consequences should be carried out in a hospital under strict medical supervision. Physiological yellowness in most cases can go away without treatment. With a pronounced degree of physiological jaundice, you can help your child with the following activities:

1. The main and main medicine is maternal colostrum, which has a laxative effect and helps to remove bilirubin from the blood of a newborn.
2. Phototherapy is often prescribed. After exposure to a special lamp, bilirubin is excreted from the child's body in 10-11 hours.
3. The sun's rays are also an excellent treatment. While walking with the child in warm weather, leave him naked for a while in the lace shade of the trees. At home, it is advisable to put the baby's cot closer to the window.
4. If the child has a pronounced jaundice, more intensive treatment is necessary. Usually, doctors prescribe activated charcoal or Smecta inside (more details in the article:). Activated carbon absorbs bilirubin, and Smecta stops its circulation between the liver and intestines.

In conclusion, it can be noted that jaundice in newborns is quite common and in the vast majority of cases passes spontaneously. Children's doctor Yevgeny Komarovsky believes that the main thing is to monitor the symptoms. Let's listen to what Komarovsky talks about this phenomenon in the next video.

The jaundice of newborns is usually called the physiological or pathological condition of the child, in which his skin becomes icteric. This condition develops against the background of the active intake of bilirubin in the tissue, due to this, the skin becomes stained yellow. A similar pigment is formed due to the breakdown of red blood cells from the body and is eliminated as a result of the activity of enzymes produced by the liver. In newborns, enzymes are excreted slowly, because a sufficient amount of them remains in the body.

And now let's dwell on this in more detail.

What is jaundice?

Staining of the skin in yellow appears against the background of an increase in the concentration of bilirubin in the blood of a newborn. Bilirubin is deposited in the skin and mucous membranes, against this background they acquire a jaundice.

After decay, the substance is excreted from the human body with the participation of enzymes that are formed in the liver. In the normal course of circumstances in the human body, cells are constantly updated, and such a process is not accompanied by jaundice. The substance is eliminated from the patient's body along with urine and feces.

In modern medicine, two types of bilirubin are distinguished:

1. Direct - water soluble and non-toxic.
2. Indirect - unbound, fat soluble, toxic.

The process of excretion and formation of bilirubin in the body of a newborn proceeds according to a different scheme. There are a number of some physiological features that can lead to a sharp increase in the concentration of indirect bilirubin. In this case, the skin of the newborn takes on a characteristic icteric hue.

The list of factors that can provoke the appearance of such a state can be represented as follows:

• active decay of red blood cells during the neonatal period;
• immaturity of the enzymatic systems of the liver;
• decrease in protein concentration in the blood;
• thinness of the skin and all its layers.

It is worth noting that physiological jaundice occurs in 100% of newborns, it develops 3-7 days after birth, but its clinical symptoms are recorded only in 60%. This is due to the fact that in some cases, symptoms are less active.

The following symptoms are characteristic of physiological jaundice:

• yellowing appears 2-7 days after birth;
• symptoms increase within 5-6 days;
• after 1 week the symptoms subside, the skin returns to a natural shade.

The orange tint inherent in the pathological state completely disappears 2-3 weeks after the appearance.

It is worth noting that jaundice in small and premature babies can proceed according to a different scheme. Often the disease has a wave-like course, the symptoms are completely eliminated a month after the onset.

The general condition of the child does not change, such jaundice does not provoke changes in the size of the liver and spleen, is not contagious. The condition does not require medical intervention.

What does jaundice look like in newborns with a photo

The main and most characteristic symptom of the disease - yellowing of the skin is difficult to notice with the naked eye. It is worth noting that not only the skin turns yellow, but also the sclera of the eyes - they become lemon. Other symptoms of physiological jaundice are not visible and after 2 weeks the skin of the newborn, again takes on a natural tone.

When jaundice occurs, it is mandatory to consult a pediatrician. Doctor
take blood for analysis to determine the rate of bilirubin in the blood. The diagnosis is determined after assessing the condition of the child and comparing it with the data of laboratory samples.

The following symptoms may be alarming:

• yellowing of the skin appears on the day the baby is born, that is, immediately after birth;
• yellowing has an upward flow;
• after a few days, the shade of the skin remains invariably yellow;
• the manifestation of green inclusions is possible;
• blanching feces;
• dark urine;
• the appearance of bruises and bruises on the body;
• an increase in the size of the liver and spleen;
• constant drowsiness, the child becomes lethargic;
• refusal to eat.

Symptoms of jaundice can have a wavy character - a sudden appearance and complete disappearance. The manifestation of these signs suggests that you can’t hesitate in contacting a doctor. The condition of the newborn can rapidly deteriorate, leading to irreversible consequences.

Causes of Jaundice

During the life of a child inside the womb, his body is provided with oxygen by red blood bodies - red blood cells. After birth, the baby begins to breathe on its own, and red blood cells with hemoglobin are no longer needed. Such elements are destroyed independently, and in the process of their destruction, bilirubin is produced, capable of staining the skin in yellow. Such an substance is excreted from the body along with urine and feces.

Jaundice in a newborn is a natural phenomenon - this is a kind of reaction of the child's body, confirming that he is only learning to live independently. The baby’s liver during this period is not mature and it is not able to process all incoming bilirubin in the required volumes, respectively, it penetrates the blood. As the filter organ grows and develops, its ability to process such a substance increases. That is why the intensity of the manifestation of physiological jaundice decreases already by 5-6 days. After reducing the intensity of the increase in the symptom, the causes for panic disappear - the liver performs its function in the required volumes.

The list of reasons that increase the likelihood of developing jaundice can be represented as follows:

• early age of mother;
• multiple pregnancy;
• at the mother;
• premature birth;
• severe iodine deficiency;
• lack of nutrients during pregnancy;
• taking certain medications during the gestation period.

The factors presented in the list are able to increase the risk of jaundice in a newborn.

Symptoms of jaundice in newborns

The clinical picture characteristic of the jaundice of a newborn can look as follows:

• yellowing of the skin;
• yellowing of the sclera of the eyes and mucous membranes;
• the probability of a change in the color of feces is not excluded;
• symptoms of anxiety, anxiety;
• loss of appetite;
• increased hemoglobin concentration in the blood;
• the development of anemia.

With pathological jaundice, an increase in the size of the liver and spleen is possible. Often there is an increase in the size of the veins of the anterior abdominal wall.

If the condition of the child does not normalize within two weeks, you should consult a doctor for a second consultation. Before proceeding with the treatment of the disease, it is important to identify an indicator of the concentration of bilirubin in the blood. The bilirubin concentration indicator depends on many factors, therefore, after receiving the examination data, the specialist will be able to accurately establish the nature of the pathology in the newborn.

Types of Jaundice

Physiological jaundice, unlike pathological jaundice, is not dangerous for the child. Physiological jaundice is diagnosed in the vast majority of newborns.

You can express a suspicion about the development of the disease in the following cases:

• yellowing of the skin can be seen several hours after childbirth;
• bilirubin concentrations become extremely high and reach 256 μmol / l;
• constant drowsiness or chaotic movements;
• discoloration of urine and feces: urine is darker, and feces are lighter.

Therapeutic intervention should be immediate. In the absence of timely reactions, bilirubin penetrates the child’s nervous system, gradually poisoning it - the development of nuclear jaundice is possible.

The clinical picture of this condition may be as follows:

• monotonous scream;
• convulsive syndrome;
• decrease in pressure indicators;
• coma.

Nuclear jaundice often develops in premature infants.

Treatment of jaundice in newborns

With pathological jaundice in a newborn, treatment is performed in a hospital. Hospitalize a woman in labor with her child. If the mother and the newborn have a Rhesus conflict, a blood transfusion of the child is performed. During 1 procedure, 70% of the blood volume is replaced. In severe cases, the blood transfusion procedure can be repeated several times.

With physiological jaundice, specific treatment is not required. Recommendations that allow you to quickly normalize well-being, are as follows:

• i recommend a newborn to be applied to the breast immediately after birth;
• the child should be exclusively breastfed, it is worth abandoning adapted mixtures;
• a woman during lactation should follow a diet, but nutrition should be balanced;
• regular walks in the sun.

As an additional method of treatment, experts recommend using phototherapy. For the procedure, the child’s eyes are covered with a special bandage. The course of therapy consists of 96 hours. During the intervention, the child may manifest various symptoms, namely peeling and a rash on the skin. In rare cases, gastrointestinal tract disorders are possible.

With severe physiological jaundice, experts may recommend the use of sorbents. Such products absorb harmful substances, including excess bilirubin. The adsorbent is designed to accelerate the process of elimination of harmful, toxic substances from the body of the child along with feces. Parents should remember that self-medication in this case is unacceptable and can cause the development of dangerous consequences. The treatment regimen and dosage of drugs are determined by a specialist individually.

The consequences of jaundice

With pathological jaundice, it is difficult to make a prognosis for recovery. The speed of recovery largely depends on the causes of the development of pathology and the severity of the pathological process. Parents should monitor the condition of the baby on the first day after birth constantly. If symptoms of jaundice appear, you should seek emergency medical attention. Particular attention should be paid to a newborn who has received birth injuries.

When the first signs of pathological jaundice appear, you need to act. The child should be shown to a specialist. Constant monitoring of the condition and adequate treatment will help to avoid the development of dangerous consequences.

In some cases, the cause of jaundice is the use of mother's milk. In this case, the reason for the increase in bilirubin in the blood of the child will be eliminated immediately after the termination of breastfeeding. Some experts do not recommend interrupting the hepatitis B; doctors advise monitoring the bilirubin in the blood of the mother and child to prevent the development of dangerous complications. Breastfeeding is recommended to be stopped only when the indicators reach critical levels.

Physiological jaundice, unlike pathological jaundice, proceeds without consequences and does not affect the development of the child's body in the future. For patients with pathological jaundice, the risk of developing cirrhosis and liver cancer increases. The vast majority of newborns in adulthood will encounter various disorders in the work of the body. The toxic effect of bilirubin on the nervous system may be irreversible. Patients may experience deafness, complete paralysis, or severe mental retardation.