GBN disease. Prevention of physiological jaundice in newborns

Hemolytic disease of the newborn (HDN) – pathological condition child (fetus), which is accompanied by the breakdown (hemolysis) of red blood cells due to the incompatibility of its blood with the mother’s blood in terms of erythrocyte antigens.

general information

Red blood cells are red cells that are the building blocks of human blood. They perform very important function: deliver oxygen from the lungs to the tissues and carry out reverse transport of carbon dioxide.

On the surface of red blood cells there are agglutinogens (antigen proteins) of two types A and B, and the blood plasma contains antibodies to them - agglutinins α and ß - anti-A and anti-B, respectively. Various combinations of these elements serve as the basis for distinguishing four groups according to the AB0 system:

• 0(I) – both proteins are absent, there are antibodies to them;
• A (II) – there is protein A and antibodies to B;
• B (III) – there is protein B and antibodies to A;
• AB (IV) – there are both proteins and no antibodies.

There are other antigens on the membrane of red blood cells. The most significant of them is antigen D. If it is present, it is considered that the blood has positive Rh factor(Rh+), and in the absence - negative (Rh-).

The blood group according to the ABO system and the Rh factor is of great importance during pregnancy: conflict between the blood of mother and child leads to agglutination (gluing) and subsequent destruction of red cells, that is, to hemolytic disease of the newborn. It is found in 0.6% of children and without adequate therapy leads to serious consequences.

Causes

The cause of hemolytic disease of newborns is a conflict between the blood of the child and the mother. It occurs under the following conditions:

• a woman with Rh-negative (Rh-) blood develops a Rh-positive (Rh+) fetus;
• the expectant mother’s blood belongs to group 0(I), and the child’s blood belongs to A(II) or B(III);
• there is a conflict regarding other antigens.

In most cases, HDN develops due to Rh conflict. There is an opinion that incompatibility according to the AB0 system is even more common, but due to mild course pathologies are not always diagnosed.

Rh conflict provokes hemolytic disease of the fetus (newborn) only under the condition of previous sensitization (increased sensitivity) of the body of matter. Sensitizing factors:

• transfusion of Rh+ blood to a woman with Rh-, regardless of the age at which it was performed;
• previous pregnancies, including those terminated after 5-6 weeks - the risk of developing tension-type headache increases with each subsequent birth, especially if they were complicated by placental abruption and surgical interventions.

With hemolytic disease of newborns with blood group incompatibility, sensitization of the body occurs in everyday life - when consuming certain foods, during vaccination, as a result of infections.

Another factor that increases the risk of pathology is a violation of the barrier functions of the placenta, which occurs as a result of the presence chronic diseases in a pregnant woman poor nutrition, bad habits and so on.

Pathogenesis

The pathogenesis of hemolytic disease of newborns is associated with the fact that the immune system the woman perceives the blood elements (red blood cells) of the fetus as foreign agents and produces antibodies to destroy them.

In case of Rh-conflict, Rh-positive erythrocytes of the fetus penetrate into the blood of the mother with Rh-. In response, her body produces anti-Rh antibodies. They pass through the placenta, enter the baby’s blood, bind to receptors on the surface of his red blood cells and destroy them. At the same time, the amount of hemoglobin in the fetal blood significantly decreases and the level of unconjugated (indirect) bilirubin increases. This is how anemia and hyperbilirubinemia (hemolytic jaundice of newborns) develop.

Indirect bilirubin is a bile pigment that has a toxic effect on all organs - kidneys, liver, lungs, heart, and so on. At high concentrations, it is able to penetrate the barrier between the circulatory and nervous systems and damage brain cells, causing bilirubin encephalopathy (kernicterus). The risk of brain damage from hemolytic disease of the newborn increases if:

• reducing the level of albumin - a protein that has the ability to bind and neutralize bilirubin in the blood;
• hypoglycemia – glucose deficiency;
• hypoxia – lack of oxygen;
• acidosis - increased blood acidity.

Indirect bilirubin damages liver cells. As a result, the concentration of conjugated (direct, neutralized) bilirubin in the blood increases. Insufficient development in a child bile ducts leads to poor excretion, cholestasis (stagnation of bile) and hepatitis.

Due to severe anemia in hemolytic disease of the newborn, foci of extramedullary (extramedullary) hematopoiesis may occur in the spleen and liver. As a result, these organs enlarge, and erythroblasts—immature red blood cells—appear in the blood.

The products of hemolysis of red blood cells accumulate in organ tissues, metabolic processes are disrupted, and a deficiency of many minerals– copper, cobalt, zinc, iron and others.

The pathogenesis of HDN in blood group incompatibility is characterized by similar mechanism. The difference is that proteins A and B mature later than D. Therefore, the conflict poses a danger to the baby towards the end of pregnancy. In premature babies, red blood cell breakdown does not occur.

Symptoms

Hemolytic disease of newborns occurs in one of three forms:

• icteric – 88% of cases;
• anemic – 10%;
• edematous – 2%.

Signs of the icteric form:

• jaundice - a change in the color of the skin and mucous membranes as a result of the accumulation of bilirubin pigment;
• decreased hemoglobin (anemia);
• enlargement of the spleen and liver (hepatosplenomegaly);
• lethargy, decreased reflexes and muscle tone.

In case of Rhesus conflict, jaundice occurs immediately after birth, in the ABO system - on the 2-3rd day. The skin tone gradually changes from orange to pale lemon.

If the level of indirect bilirubin in the blood exceeds 300 µmol/l, nuclear hemolytic jaundice may develop in newborns on days 3-4, which is accompanied by damage to the subcortical nuclei of the brain. Kernicterus is characterized by four stages:

• Intoxication. It is characterized by loss of appetite, monotonous screaming, motor weakness, and vomiting.
• Nuclear damage. Symptoms – tension occipital muscles, sharp cry, swelling of the fontanelle, tremor, (posture with arching of the back), disappearance of some reflexes, .
• Imaginary well-being (improved clinical picture).
• Complications of hemolytic disease of the newborn. Appear at the end of the 1st – beginning of the 5th month of life. Among them are paralysis, paresis, deafness, cerebral palsy, developmental delay, and so on.

On days 7-8 of hemolytic jaundice, newborns may experience signs of cholestasis:

• stool discoloration;
• greenish-dirty skin tone;
• darkening of urine;
• an increase in the level of direct bilirubin in the blood.

In anemic form clinical manifestations hemolytic disease of newborns include:

• anemia;
• pallor;
• hepatosplenomegaly;
• slight increase or normal bilirubin level.

The anemic form is characterized by the mildest course - the child’s general well-being almost does not suffer.

The edematous variant (intrauterine hydrops) is the most severe form of HDN. Signs:

• pallor and severe swelling of the skin;
• big belly;
• pronounced enlargement of the liver and spleen;
• muscle flaccidity;
• muffled heart sounds;
• breathing disorders;
• severe anemia.

Edema hemolytic disease of the newborn leads to miscarriages, stillbirths and death of children.

Diagnostics

Diagnosis of tension-type headache is possible in the prenatal period. It includes:

1. Collecting anamnesis - clarifying the number of previous births, miscarriages and transfusions, finding out information about the health status of older children,
2. Determination of the Rh factor and blood group of the pregnant woman, as well as the father of the child.
3. Mandatory detection of anti-Rh antibodies in the blood of a woman with Rh- at least 3 times during the period of bearing a child. Sharp fluctuations in numbers are considered a sign of conflict. In case of incompatibility with the AB0 system, the titer of allohemagglutinins is monitored .
4. Ultrasound scan - shows thickening of the placenta, polyhydramnios, enlargement of the fetal liver and spleen.

If there is a high risk of hemolytic disease of the newborn, amniocentesis is performed at 34 weeks - the collection of amniotic fluid through a puncture in the bladder. In this case, the density of bilirubin, the level of antibodies, glucose, iron and other substances are determined.

After birth, the diagnosis of HDN is made based on clinical symptoms And laboratory research. A blood test shows:

• bilirubin level is above 310-340 µmol/l immediately after birth and its increase by 18 µmol/l every hour;
• hemoglobin concentration below 150 g/l;
• decrease in the number of red blood cells with a simultaneous increase in erythroblasts and reticulocytes ( immature forms blood cells).

A Coombs test is also performed (shows the number of incomplete antibodies) and the level of anti-Rhesus antibodies and allohemagglutinins in the mother’s blood and breast milk is monitored. All indicators are checked several times a day.

Hemolytic disease of newborns is differentiated from anemia, severe asphyxia, intrauterine infection, physiological jaundice and other pathologies.

Treatment

Treatment of severe hemolytic disease of newborns in the prenatal period is carried out by transfusion of red blood cells into the fetus (through the umbilical cord vein) or with the help of exchange blood transfusion (BRT).

ZPK is a procedure for alternately removing the child’s blood in small portions and introducing donated blood. It removes bilirubin and maternal antibodies while replenishing lost red blood cells. Today, for PCD, not whole blood is used, but red blood cells mixed with frozen plasma.

Indications for PCP for full-term infants diagnosed with hemolytic jaundice of newborns:

• bilirubin in cord blood above 60 µmol/l and an increase in this indicator by 6-10 µmol/l every hour, the pigment level in the peripheral blood is 340 µmol/l;
• hemoglobin is below 100 g/l.

In some cases, the procedure is repeated after 12 hours.

Other methods used to treat TTH in newborns:

• hemosorption - filtration of blood through sorbents that cleanse it of toxins;
• plasmapheresis – removal of part of the plasma along with antibodies from the blood;
• administration of glucocorticoids.

Treatment of tension-type headache in mild to moderate cases, as well as after PCD or blood cleansing includes medications and phototherapy.

Medicines used for hemolytic disease of the newborn:

• protein preparations and glucose intravenously;
• liver enzyme inducers;
• vitamins that improve liver function and activate metabolic processes - E, C, group B;
• choleretic agents in case of thickening of bile;
• transfusion of red blood cells;
• sorbents and cleansing enemas.

Phototherapy is a procedure for irradiating a child’s body with a fluorescent lamp with white or blue light, during which indirect bilirubin found in the skin is oxidized and then eliminated from the body.

Attitudes towards breastfeeding during HDN in newborns are ambiguous. Previously, it was believed that a baby could be put to the breast only 1-2 weeks after birth, since by this time there were no antibodies in the milk. Today, doctors are inclined to start breastfeeding from the first days, since anti-Rh antibodies are destroyed in the baby’s stomach.

Forecast

The consequences of hemolytic disease of newborns depend on the nature of the course. A severe form can lead to the death of the child in the last months of pregnancy or within a week after birth.

If bilirubin encephalopathy develops, complications such as:

• cerebral paralysis;
• deafness, blindness;
• developmental delay.

Previous hemolytic disease of newborns at an older age provokes a tendency to frequent illnesses, inadequate reactions to vaccination, allergies. Adolescents experience decreased performance, apathy, and anxiety.

Prevention

Prevention of hemolytic disease of newborns is aimed at preventing sensitization of women. The main measures are blood transfusions only taking into account the Rh factor, preventing abortions, and so on.

Since the main sensitizing factor for Rh conflict is previous births, within 24 hours after the birth of the first child with Rh+ (or after an abortion), the woman must be administered a drug with anti-D immunoglobulin. Thanks to this, fetal red blood cells are quickly removed from the mother’s bloodstream and do not provoke the formation of antibodies in subsequent pregnancies. An insufficient dose of the drug or its late administration significantly reduces the effectiveness of the procedure.

Prevention of HDN during pregnancy when Rh sensitization is detected includes:

• nonspecific hyposensitization - administration of detoxification, hormonal, vitamin, antihistamine and other drugs;
• hemosorption, plasmapheresis;
• specific hyposensitization - transplantation of a skin flap from the husband;
• PCP at 25-27 weeks followed by emergency delivery.

Hemolytic disease of the fetus and newborn

Hemolytic disease of the newborn- a disease that is caused by incompatibility between the blood of mother and fetus for various antigens that are present in the blood of the newborn (inherited from the father) and which are absent in the blood of the mother.

Most often it develops if the blood of the mother and fetus is incompatible with the Rh antigen (1 case in 200-250 births). Rhesus bodies according to Wiener have several types - Rh0, Rh", Rh". According to the proposal of Fischer-Reiss, the types of Rh antigen began to be designated respectively by the letters D, E and C. Typically, a Rh conflict develops with incompatibility for Rh0, i.e. (D) antigen, and less often for other types. The cause of hemolytic disease may also be incompatibility with ABO system antigens.

Anti-Rh antibodies are formed in 3-5% of women with Rh-negative blood during pregnancy with a fetus with Rh + blood.

During the first pregnancy, children with Rhesus conflict are born less often; this is more common during the second or third. If ABO is incompatible, the disease can develop during the first pregnancy.

Hemolytic disease of newborns can manifest itself in the following ways:

1. the child dies during intrauterine development(at 20-30 weeks);

2. born with universal edema;

3. in the form of early-onset severe jaundice or

4. severe anemia.

Changes in the fetal body during HMB

Hyperbilirubinemia does not have much effect on the condition of the fetus because the mother's liver functions to neutralize the bilirubin that is formed. Hyperbilirubinemia is dangerous for the newborn.

A fetus with a non-molytic disease exhibits dropsy with abdominal bloating, subcutaneous edema, anemia with a predominance of immature forms of red blood cells, ascites, enlarged liver and spleen, dilated heart cavities, hydrothoracmus, plethora in the lungs, erythropoiesis in the kidneys, and polycythemia in the bone marrow. The placenta is edematous, enlarged, often up to 50% of the fetal size, yellow color due to pigments secreted by the fetal kidneys.

Hemolytic disease often develops in the newborn– during the birth process, maternal antibodies enter the bloodstream before the umbilical cord is crossed.

After birth, toxic indirect accumulates in the tissues of the newborn. In the cells of the nervous system, the processes of cellular respiration are disrupted.

The following options for the penetration of antibodies through the placenta are possible:

1. during pregnancy, which leads to congenital forms of HDN

2. during childbirth, which leads to the development of postpartum icteric form;

To diagnose GMB in a newborn, immediately after birth, tests are taken to determine the child’s blood type, Rh factor, hemoglobin, bilirubin content, and red blood cell count. Normally, hemoglobin is 38.4 g/l, bilirubin is 11.97-47.88 μmol/l, red blood cells are 6.0 10|2/l

Forms of hemolytic disease of the newborn

Hemolytic anemia - most light form. The newborn's hemoglobin level is reduced, as is the number of red blood cells. The skin is pale, the liver and spleen are slightly enlarged. The content of hemoglobin and bilirubin is at the lower limit of normal. The anemic form of GMB appears due to the effect of a small amount of Rh antibodies on a full-term or almost full-term fetus. Isoimmunization of the fetus occurs more often during childbirth. The main symptom of mild injury is anemia.

Hemolytic anemia in combination with jaundice– occurs more frequently and is characterized as a more severe form of the disease.Characterized by hyper- or normochromic anemia, jaundice and hepatosplenomegaly. Amniotic fluid is jaundiced, as are vernix, umbilical cord, membranes and umbilical cord. The content of indirect bilirubin is higher upper limit norms are 10-20 µmol/l. The newborn's condition is serious and worsening. If the hourly increase in bilirubin is 5-10 times, then “ kernicterus", which indicates damage to the central nervous system. In such cases, blindness, deafness, and mental disability may occur. The hemoglobin content is below normal. The icteric form occurs if antibodies act on a mature fetus for a short time. Infectious complications are often associated - pneumonia, respiratory distress syndrome, omphalitis. After 7 days of life, the pathogenic effect of antibodies entering the fetal blood ceases.

Hemolytic anemia in combination with jaundice and dropsy– the most severe form of the disease. Newborns are either stillborn or die in the early neonatal period. Symptoms of the disease are: anemia, jaundice and general edema (ascites, anasarca), severe splenomegaly. May develop hemorrhagic syndrome. The penetration of maternal antibodies through the placenta does not always occur; the severity of damage to the fetus does not always correspond to the titer (concentration) of Rh antibodies in the blood of a pregnant woman.

Treatment of fetal GMB

Intrauterine blood transfusions are performed under ultrasound control after the 18th week of pregnancy. Intrauterine blood transfusion gives a chance for pregnancy.

Based on the technique used, blood transfusion is divided into:

Intra-abdominal– carried out up to 22 weeks of pregnancy,or if intravascular transfusion is not possible. The abdominal cavity, the wall of the uterus, and the abdominal cavity of the fetus are pierced. Single-group and Rh-negative red blood cells are administered. After absorption lymphatic system reaches the fetal vascular system. They also take samples to determine blood type, Rh factor, fetal karyotype, and hemoglobin.

Intravascular- cordocentesis is performed. The umbilical cord vein is pierced near the entrance of the placenta, blood is collected for tests (the hematocritical number of the fetus is determined), red blood cells are administered, and blood is again collected for tests and to evaluate the therapy performed. The components are transfused directly into the blood of the fetus, which saves his life if the outcome is favorable.

L Treatment of hemolytic disease of the newborn

The following methods are most effective:

1. exchange transfusion to the newborn, as a result of which Rh antibodies and bilirubin are excreted. An increase in the antibody titer in the mother during pregnancy to 1:16 or higher should alert the neonatologist regarding GMB in the newborn. It is most unfavorable when antibodies decrease before birth, indicating that they have transferred to the fetus. Severe form Hemolytic disease can be assumed in the presence of icteric discoloration of the skin, cheese-like lubricant, placenta, amniotic fluid, swelling and enlargement of the fetal liver.

Risk factors for bilirubin encephalopathy include:

o low weight of the newborn – less than 1500 g.

o Low content total protein less than 50 g/l - - hypoproteinemia

o Low glucose level – less than 2.2 mmol/l - hypoglycemia

o Low hemoglobin content – ​​less than 140 g/l - anemia

o Intrauterine infection of the fetus, the appearance of jaundice on the first day

Indications for exchange blood transfusion:

o the appearance of jaundice immediately after birth or in the first hours of life;

o rapid hourly increase in bilirubin in the first hours of life 6.8 mmol/l

o hemoglobin level below 30 g/l.

For replacement blood transfusion, single-group or 0(1) group Rh-negative red blood cells and plasma [single-group or AB(IV)] are used.

In case of conflict according to the AB0 system, the red blood cell mass must be 0(1) group, suspended in plasma of the AB(IV) group. In case of blood incompatibility due to rare factors, individual selection of donors is carried out.

40-50 ml of blood is removed from the newborn and the same amount of red blood cells is injected. When repeating replacement transfusions, the dose is reduced by 2 times. The total volume of red blood cells is 70 ml per 1 kg of the child’s body weight.

Exchange blood transfusion is effective for removing toxic hemolysis products, indirect bilirubin, antibodies and under-oxidized metabolic products from the newborn's body. Possible complications: heart failure, air embolism, infection, anemia, hemorrhagic syndrome.

2. Phototherapy- irradiation of the newborn using a fluorescent lamp Phototherapy promotes the conversion of free bilirubin in the skin and capillaries into non-toxic metabolites (biliverdin), which are excreted in the urine and bile of the fetus. In this case, albumins lose their ability to bind bilirubin. Light penetrates the newborn's skin to a depth of 2 cm.

Indications for phototherapy:

o conjugation jaundice (in full-term newborns) with indirect bilirubin in the serum up to 170-188 µmol/l

o hemolytic disease of the newborn due to Rh factor and group incompatibility;

o condition after exchange blood transfusion in severe form of hemolytic disease;

o prevention in newborns at risk for the development of hyperbilirubinemia (perinatal hypoxia, immature and premature newborns, impaired thermoregulation).

Newborns may develop toxic effects - erythema, dispensation, burns, hypohydration. Stops when direct bilirubin values ​​exceed 85 µmol/l.

3. Therapy with intravenous immunoglobulins. Immunoglobulins in high doses block Fc receptors, which are involved in cytotoxic reaction antigen - antibody and thereby reduce hyperbilirubinemia.

Newborns are administered intravenously ImBio-immunoglobulins at a dose of 800 mg/kg per day for 3 days. Combined with phototherapy.

TOComplex therapy for newborn HMB- exchange blood transfusion, phototherapy and intravenous administration immunoglobulin - reduces the frequency and severity of pathology, improves the prognosis of children's development.

It is believed that after the first pregnancy with an Rh-positive fetus, sensitization occurs in 10% of Rh-negative women. With each subsequent pregnancy, 10% are immunized with an Rh-positive fetus.

Out of 1000 people giving birth, 170 will have a rhesus negative blood. Of these, 100 women will have a child who is Rh positive.

With strict implementation of the method of specific prevention of Rh sensitization, the problem of Rh conflict pregnancy can be practically solved.

Take care of yourself!

Hemolytic disease of newborns (HDN) appears against the background of incompatibility of the mother’s blood with the blood of the gestating fetus due to a number of conditions.

Malaise with hemolytic disease of newborns according to blood group (HDN) is extremely serious, because it often forms during intrauterine period and has the ability to take on different forms.

The result of the neglected condition is the same - the destruction of red blood cells and the death of the child.

Hemolysis is destruction of the red blood cell membrane with the release of hemoglobin in plasma. This process is normal, because after 120 days it ends the life period of the red blood cell. However, if pathological destruction occurs under the established conditions, the entire mechanism of activity is disrupted circulatory system. Freed hemoglobin in large number when it enters the plasma, it will be poisonous, because it overloads the body with a large amount of bilirubin, etc. In addition, it leads to the formation of anemia.

Removing bilirubin from the body

If a lot of bilirubin is released in a toxic form, those organs that are directly involved in its reconstruction and excretion suffer. Bilirubin from the blood enters the liver, where its conjugation takes place, in other words, destruction. However, if there is a lot of it, the liver simply does not have time to process the huge amount. As a result, the neurotoxic form of this particular pigment migrates from one organ to another, inhibiting oxidative processes and initiating destructive changes in tissues and organs at the cell level, up to their destruction.

At a concentration greater than 340 μmol/L, bilirubin will pass through a special blood-brain barrier, changing the structure of the brain. For premature babies, only a concentration of 200 µmol/l is enough. Thus, bilirubin encephalopathy is formed, which poisons the brain and leads to further disability. The disease is also characterized by the so-called extramedullary hematopoiesis - movements in which blood is formed not in the tissues bone marrow, and in other organs. Because of this, organ enlargement occurs, simultaneously with a lack of such important microelements as zinc, iron and copper. Erythrocyte destruction elements “settle” in the cells of the pancreas, kidneys and other organs.

Reasons for the formation of HDN

The cause of the progress of hemolytic disease, as a rule, is the mismatch between the mother’s blood and the child’s Rh. . However, even with such formed genes or due to ABO-conflict combinations (we will thoroughly examine the essence of the problem today), the destruction of red blood cells occurs in no more than 6 cases out of 100. This means that it makes sense to fight for the existence of the baby, and effective ways there are cures. Let's talk in more detail about common blood incompatibilities.

ABO conflicts

As established, according to the ABO system there are 4 combinations that make up 4 blood groups. So, if the mother has group I, and the baby has group II, either III group, an immunoconflict is likely. Although it is generally accepted that “hostility” according to the ABO system occurs more often than rhesus conflict, the disease of newly born children in this case is much easier. Sometimes it is barely visible, so it cannot always be diagnosed.

Rhesus conflict

The Rh factor can be either positive or negative, and is noted as Rh+ and Rh-, respectively. The existence or lack of this condition (antigen D on the surface of the red blood cell) does not affect the condition in any way the health of its owner and life itself. But with the exception of one situation: if we are not talking about a mother with Rh negative who wants to have children from an Rh positive father. In this case, the risk of a complicated pregnancy increases. Rh conflict expresses itself if a woman has negative blood, and her baby is Rh-positive.

Where does such hostility come from? During the period of impact positive blood of the fetus in the direction of the blood of the mother with negative Rh, the woman’s immunity gives an alarm about the penetration of “strangers”, since the body is unfamiliar with the Rh protein. Antibodies are formed aimed at eliminating the “enemy”, which will be the blood of your baby! The first pregnancy, as a rule, proceeds without difficulties, because the maternal immune system is not yet sensitized and antibodies are formed in small numbers.

However, there are conditions in which the risk of conflict is high. These include:

• second and subsequent births;
• ectopic pregnancy;
• 1 pregnancy ended in miscarriage or abortion;
• transfusion of previously positive blood, besides, the statute of limitations does not matter.

There are conditions when mother and baby become “enemies.” The consolation in this case is that 85% of people with fair skin are Rh positive.

The nature and symptoms of the disease in newborns

There are several forms of hemolytic disease:

Diagnosis of the disease

When registering a pregnant woman, first of all, her blood type and Rh are determined. Expectant mothers with negative Rh are under the attention of obstetricians. A similar study is underway future dad. A woman is asked about former pregnancies how they proceeded, whether there were miscarriages or not, termination of pregnancy, etc.

A pregnant woman definitely needs to be checked in a timely manner and take the required tests. For Rh-negative mothers, blood is taken at least 3 times during pregnancy to check the titer of anti-Rhes antibodies. If there is concern that there is an immunoconflict, a special amniocentesis is performed. This is a method of studying amniotic fluid, thanks to which information is obtained about the density of bilirubin in the fetus and the concentration of other elements. Sometimes they resort to cordocentesis.

When conducting an ultrasound examination, special attention is paid to the thickening of the placenta, the rate of its increase, the presence of polyhydramnios, ascites, enlargement of the boundaries of the liver and spleen. All together can indicate swelling of the placenta and the formation of hemolytic disease. Cardiotocography makes it possible to evaluate cardiac activity and detect possible hypoxia. After birth, diagnosis of the disease is based on obvious manifestations (jaundice, anemia) and these results over time. For example, the content of bilirubin, hemoglobin in umbilical cord blood, and the presence or absence of erythroblasts are assessed.

Treatment of newborns

The main goal in case of manifestations of the disease will be antitoxic therapy; in this case, there is removal from the child’s body. toxic substances, namely bilirubin. Phototherapy is extremely effective. The method is based on observations, according to which, under the influence of daylight, jaundice (a sign of hyperbilirubinemia) is significantly reduced due to the destruction and excretion of unconjugated bilirubin.

To perform the procedure, fluorescent lamps with blue, white and blue light are used. When determining phototherapy sessions, they take into account not only the bilirubin level, but also body weight, and, in addition, the age of the newborn. During the session, the child stays either in a special bed or in an incubator. Any 12 hours is done blood collection to monitor bilirubin.

After the widespread use of phototherapy, the need for blood transfusions decreased by almost 40%, the walking time of children with jaundice was reduced, and there were certainly fewer complications. The treatment, in addition, contains the normalization of liver activity through the introduction of vitamins B, E, C, and cocarboxylase. They make metabolism movements better. Choleretic agents can help combat thickening of bile, and cleansing enemas and the use of activated carbon inhibits the absorption of bilirubin in intestinal tract. A unified detoxification therapy is being carried out.

Phototherapy is extremely an effective way to combat jaundice. In difficult moments (the formation of anemia), therapy is carried out quickly, with the support of blood transfusion or its elements, for example, red blood cells. In this case, the Rh affiliation of the fetus is provided.

Is it possible to breastfeed babies?

Previously, breastfeeding children in the presence of conflict or hemolytic disease existed banned, later the baby was allowed to be put to the breast only 2 weeks after birth.

It was believed that anti-Rh antibodies in milk were ready to harm the infant. It has now been confirmed that, upon penetrating the digestive tract, they are destroyed under the influence of of hydrochloric acid and enzymes, therefore, cannot enter the bloodstream and, therefore, cause harm.

Forecasts for the future

It is difficult to say how the manifestations of the disease will affect the baby in the future; it all depends on the difficulty of developing the disease. In the most unfavorable cases, a further delay in development, cerebral palsy, is observed. In situations, the hepatobiliary system suffers more easily due to high overload on it, the child is prone to allergies, special interactions with vaccinations, there may be the formation of strabismus, and difficulties with hearing.

Prevention of the condition

Prevention can be divided into 2 stages.

When the mother is not sensitized

That is, her negative blood had not previously encountered positive antigens. Such a mother should approach her first pregnancy with trepidation, since she has the highest chances of a positive result. She is strongly discouraged from having abortions and blood transfusions. In the 3rd trimester, an analysis is performed several times to detect antibodies.

When the mother is sensitized

Within 24 hours after childbirth and the birth of an Rh-positive child, immunoglobulin will turn on, the task of which is to prevent the formation of antibodies in the maternal blood. This procedure is also performed after:

• ectopic pregnancy;
• abortion;
• transfusion of Rh-positive blood;
• a kind of diagnostics in the fetus.

Another option for preventing hemolytic disease of newborns is a kind of hyposensitization. Its essence is as follows: a piece of skin from the husband (Rh +) is transplanted to the wife (with Rh -) and in this case the antibodies “switch” their attention to the graft, thereby reducing the hemolysis of red blood cells.

conclusions

As you can see, this disease has serious consequences. For this reason, it is very important for mothers with Rh-negative blood to remember their own Rh status and take the problems of motherhood and bearing a baby seriously. If the obstetrician-gynecologist declares that it is necessary to undergo auxiliary tests, it is better to do this so that the situation does not get out of control. Equally important timely treatment. In this case, the risk of hemolysis of red blood cells with all the ensuing consequences will ultimately be minimized.

When registering for pregnancy, did you see “ABO, Rh incompatibility” and “threat of HDN” in the card? How serious is this pathology and how can it affect health and mental development baby, symptoms and treatment methods for hemolytic disease of the newborn - we sought professional advice from gynecologists and pediatricians.

Hemolytic disease of the newborn(jaundice of newborns, HDN) is a pathology of the hematopoietic system of infants, which occurs due to:

• Rh-conflict with mother (Rh-conflict);
• blood group incompatibility (ABO conflict);
• less often - due to intake medications and impact negative factors during pregnancy.

In the presence of these risk factors, the mother’s immune system “scans” the baby’s blood cells as if they were foreign agents. The production of antibodies begins, they penetrate the blood-placental barrier and attack the baby’s blood segments.

If the level of antibodies in the mother’s blood is high and there is no drug correction, the fetus may die in the womb. In other cases, immediately after birth, the newborn develops symptoms of tension-type headache.

In the first hours after birth, a baby with HDN begins a massive breakdown of red blood cells. There is an increase in blood depot organs (spleen, liver), and the concentration in the blood increases sharply.

Enzymatic systems In newborns, the liver is immature and does not function sufficiently, which is why “bad”, indirect bilirubin, a breakdown product of red blood cells, accumulates in the baby’s blood. Indirect bilirubin is toxic, it damages the baby’s cardiac myocardial cells, liver hepatocytes, most affecting nervous system child.

Doctors diagnose the presence of hemolytic disease of newborns based on the following signs:

• the presence in the mother’s exchange card of data on the possibility of an Rh- or ABO-conflict with the fetus;
• yellowing of the skin - immediately at birth or in the first 24-72 hours of life;
• the baby is lethargic, eats poorly and sleeps a lot, often spits up after feeding;
• uneven breathing;
• innate reflexes decrease;
• swelling;
• enlarged lymph nodes, heart, liver or spleen;
• anemia, low level Gb (hemoglobin) in the blood;
• symptom of the “setting sun” - the child unnaturally lowers his eyes to the bottom.

In the first 3-5 days of a baby’s life, a test for HDN can be taken directly from the umbilical vein. The trend of increasing bilirubin and the presence of swelling provide information to doctors about the form of the disease and possible reason its occurrence, and also allow us to compile correct scheme treatment.

Why does hemolytic jaundice occur in infants?

Rhesus conflict occurs in a mother with negative Rh and a child with positive Rh. The first pregnancy in such cases, as a rule, proceeds without complications and a healthy baby is born. The 2nd and 3rd pregnancies already require clinical observation, because the risk of having a child with hemolytic disease increases to 85%.

ABO incompatibility most often detected in women with blood group I (0), whose husbands are carriers of blood groups II (A) and III (B). With ABO incompatibility, even the first pregnancy can have a complication in the form of HDN.

Symptoms of hemolytic disorders in a baby with different incompatibility differ in severity:

The severity of the disease largely depends on the penetration of the mother's antibodies and the duration of their effect on the fetus.

1. Sometimes the mother’s body synthesizes a small amount of antibodies; they do not penetrate the placental barrier, but affect the baby’s blood only when passing through birth canal. In this case, hemolytic jaundice does not have serious consequences for the baby and disappears without a trace after several “blue light” procedures and vitamin therapy.
2. Periodic “attack” of antibodies on the fetal hematopoietic system, their high level throughout the entire period of pregnancy lead to more serious consequences: birth of a macerated fetus, development of anemic, edematous or icteric form of HDN.

A severe form of hemolytic disease of newborns is diagnosed immediately after birth: water with HDN is yellowish or greenish in color, the child is born pale or jaundiced, traces of edema are noticeable on the baby’s body, the spleen and liver are enlarged.

Types of HDN

There are three forms of hemolytic disease of newborns: edematous, anemic and icteric.

Edema form

Is the hardest: vital important organs The baby increases significantly in size while still in the mother's womb. As a result, the baby is born with twice the normal weight, fluid may accumulate in the abdominal and pleural cavity, and the level of hemoglobin in the blood drops to 35-50 g/l.

Jaundice form of hemolytic disease

A consequence of the effect of antibodies on an already mature fetus. The baby is born full-term, without visible signs of the disease. Symptoms of jaundice in such children appear in the first 24-48 hours of life: enlargement of the lymph nodes, spleen and liver may be observed, the skin and visible mucous membranes acquire a yellowish tint.

Anemic form

It occurs most easily in newborns. Is born healthy child, by the end of the 1st week of life he may show signs of anemia - pale skin, decreased hemoglobin levels and increased bilirubin levels in the blood.

A more severe course of the disease is observed in premature infants. It is easier for the body of babies born at term to cope with the massive breakdown of red blood cells: all its systems are more mature and not so vulnerable to negative impact toxic indirect bilirubin.

Methods and drugs for the treatment of hemolytic disease

If your baby has been diagnosed with HDN, don’t despair. If provided in a timely manner medical care all processes in his small body will quickly return to normal and the risk of damage to the central nervous system will be eliminated.

Treatment of hemolytic disease is complex. It is aimed at removing antibodies and indirect bilirubin from the blood, as well as normalizing the functions of the kidneys and liver.

For Rhesus conflict breast-feeding, most likely, you will have to stop and offer your baby infant formula. Phenobarbital, methionine, prednisolone and intramuscular injections ATP.

Children with the icteric form of hemolytic disease undergo phototherapy sessions: under the influence of light, bilirubin breaks down into harmless substances.

In severe cases of HDN, blood transfusions are performed.

How to prevent hemolytic disease of the newborn in a baby?

When we meet loved one, the last thing that comes to mind is to ask about his blood type. But a mismatch of Rh factors is not a death sentence! You can give birth healthy baby, if you pay attention to the prevention of tension-type headache. For this:

• When registering with antenatal clinic Get your husband's blood tested.
• If you already know that there is incompatibility, inform the gynecologist observing the pregnancy as soon as possible.
• Monitor the level of antibodies in the blood - experts recommend undergoing such tests at least 3 times during 9 months of your “interesting” situation.
• Inform your gynecologist about the presence of aggravating factors - abortions, miscarriages and signs of central nervous system damage in older children.
• Undergo amniotic fluid testing - amniocentesis.

Jaundice is a visual manifestation of hyperbilirubinemia. Bilirubin, one of the end products of the catabolism of the heme protoporphyrin ring, accumulates in large quantities in the body and causes a yellow coloration of the skin and mucous membranes. The breakdown of 1 g of hemoglobin produces 34 mg of bilirubin. In adults it appears when the bilirubin level is more than 25 µmol/l, in full-term newborns - 85 µmol/l, and in premature infants - more than 120 µmol/l.

A transient increase in the concentration of bilirubin in the blood in the first 3-4 days after birth is observed in almost all newborns. In approximately half of full-term and most premature infants, this is accompanied by the development of icteric syndrome. An important task of a medical worker during the period of monitoring the health of a newborn child is to distinguish between physiological characteristics and pathological disorders of bilirubin metabolism.

Physiological jaundice

Clinical criteria:

appears 24-36 hours after birth;

increases during the first 3-4 days of life;

begins to fade from the end of the first week of life;

disappears in the second or third week of life;

the general condition of the child is satisfactory;

the size of the liver and spleen is not enlarged;

normal color of stool and urine.

Laboratory criteria:

concentration of bilirubin in umbilical cord blood (moment of birth) -< 51 мкмоль;

the hemoglobin concentration in the blood is normal;

maximum concentration total bilirubin on days 3-4 in peripheral or venous blood: ≤240 µmol/L in full-term infants and ≤ 150 µmol/L in premature infants;

total blood bilirubin increases due to the indirect fraction;

the relative proportion of the direct fraction is less than 10%.

Pathological hyperbilirubinemia

Present at birth or appear on the first day or second

week of life;

Combined with signs of hemolysis (anemia, high reticulocytosis, nuclear erythroid forms in the blood smear, excess spherocytes), pallor, hepatosplenomegaly;

Lasts more than 1 week. in full-term and 2 weeks. - in premature babies;

They occur in waves (the yellowness of the skin and mucous membranes increases in intensity after a period of its decrease or disappearance);

The rate of increase (increase) of unconjugated bilirubin (NB, indirect bilirubin) is >9 µmol/l/h or 137 µmol/l/day.

The level of NB in ​​umbilical cord blood serum is >60 µmol/L or 85 µmol/L in the first 12 hours of life, 171 µmol/L on the 2nd day of life, the maximum NB values ​​on any day of life exceed 221 µmol/L

The maximum level of bilirubin diglucuronide (BDG, direct biliru-

bin) - >25 µmol/l

Deterioration of the child’s general condition against the background of a progressive increase in jaundice,

Dark urine or discolored stools

Physiological jaundice is a diagnosis excluding pathological jaundice.

There are four main mechanisms for the development of pathological hyperbilirubinemia:

1. Hyperproduction of bilirubin due to hemolysis;

2. Impaired conjugation of bilirubin in hepatocytes;

3. Impaired excretion of bilirubin into the intestines;

4. Combined violation of conjugation and excretion.

In this regard, from a practical point of view, it is advisable to distinguish four types of jaundice:

1) hemolytic;

2) conjugation;

3) mechanical;

4) hepatic.

Hemolytic disease of newborns (HDN) is an isoimmune hemolytic anemia that occurs in cases of incompatibility between the blood of mother and fetus for erythrocyte antigens, while the antigens are localized to the mother and fetus, and antibodies to them are produced in the mother's body. HDN in Russia is diagnosed in approximately 0.6% of all newborns.

Classification GBN provides for the establishment of:

Type of conflict (Rh-, AB0-, other antigenic systems);

Clinical form (intrauterine death of the fetus with maceration, edematous, icteric, anemic);

Degrees of severity for icteric and anemic forms (mild, moderate and severe);

Complications (bilirubin encephalopathy - kernicterus, other neurological disorders; hemorrhagic or edematous syndrome, damage to the liver, heart, kidneys, adrenal glands, "bile thickening" syndrome, metabolic disorders - hypoglycemia, etc.);

Concomitant diseases and underlying conditions (prematurity, intrauterine infections, asphyxia, etc.)

Etiology. A conflict may arise if the mother is antigen-negative and the fetus is antigen-positive. There are 14 known main erythrocyte group systems, combining more than 100 antigens, as well as numerous private erythrocyte antigens and common erythrocyte antigens with other tissues. HDN usually causes incompatibility of the fetus and mother for Rh or ABO antigens. It has been established that the Rh antigen system consists of 6 main antigens (the synthesis of which is determined by 2 pairs of genes located on the first chromosome), designated either C, c; D, d; Ε, e (Fisher's terminology), or Rh", hr", Rho, hr0, Rh", hr" (Winner's terminology). Rh-positive red blood cells contain D-factor (Rho factor, in Winner's terminology), while so-called Rh-negative red blood cells do not. Incompatibility of ABO antigens, leading to HDN, usually occurs with the mother's blood group 0 (1) and the child's blood group A (II). If HDN develops due to double incompatibility of the child and mother, i.e. the mother is O (I) Rh(-), and the child is A (II) Rh(+) or B (III) Rh (+), then, as a rule, it is caused by A- or B-antigens. Rh-HDN is usually caused by sensitization of the Rh-negative mother to the Rh-O antigen prior to pregnancy. Sensitizing factors are, first of all, previous pregnancies (including ectopic ones and those ending in abortions), and therefore Rhesus HDN, as a rule, develops in children not born from the first pregnancy. In case of ABO-conflict, this pattern was not noted, and ABO-THB can occur already during the first pregnancy, but if the barrier functions of the placenta are impaired due to the presence of somatic pathology, gestosis, leading to intrauterine fetal hypoxia.

Pathogenesis.

Previous abortions, miscarriages, ectopic pregnancy, childbirth, etc. predispose the antigen-positive erythrocytes of the fetus to enter the bloodstream of the antigen-negative mother. In this case, the mother’s body produces anti-Rhesus or group antibodies. Incomplete anti-red blood cell antibodies, belonging to class G immunoglobulins, damage the erythrocyte membrane, leading to an increase in its permeability and metabolic disorders in the erythrocyte. These red blood cells, changed under the influence of antibodies, are actively captured by macrophages of the liver, spleen, bone marrow and die prematurely; in severe forms of the disease, hemolysis can also be intravascular. The resulting large amount of NB entering the blood cannot be eliminated by the liver, and hyperbilirubinemia develops. If hemolysis is not too intense with a small amount of incoming maternal antibodies, the liver quite actively removes NB, then in the child the clinical picture of HDN is dominated by anemia with the absence or minimal severity of jaundice. It is believed that if anti-erythrocyte alloimmune antibodies penetrated to the fetus for a long time and actively during pregnancy before the onset of labor activity, then intrauterine maceration of the fetus or an edematous form of HDN develops. In most cases, the placenta prevents the penetration of alloimmune antibodies to the fetus. At the time of birth, the barrier properties of the placenta are sharply disrupted, and maternal isoantibodies enter the fetus, which, as a rule, causes the absence of jaundice at birth and its appearance in the first hours and days of life. Anti-erythrocyte antibodies can be passed to the baby through mother's milk, which increases the severity of HDN.

Features of pathogenesis in the edematous form of HDN. Hemolysis begins from 18-22 weeks. pregnancy, is intense and leads to severe fetal anemia. As a result, severe fetal hypoxia develops, which causes deep metabolic disorders and damage to the vascular wall, a decrease in albumin synthesis occurs, albumin and water move from the fetal blood to the tissue interstitium, which forms a general edematous syndrome.

Features of pathogenesis in the icteric form of HDN. Hemolysis begins shortly before birth, the level of bilirubin quickly and significantly increases, which leads to its accumulation in the lipid substances of tissues, in particular in the nuclei of the brain, an increase in the load on liver glucuronyltransferase and an increase in the excretion of conjugated (direct) bilirubin, which leads to impaired bile excretion .

Features of the pathogenesis of the anemic form of HDN. The anemic form of HDN develops when small amounts of maternal antibodies enter the fetal bloodstream shortly before birth. At the same time, hemolysis is not intense, and the newborn’s liver quite actively removes bilirubin.

Although hyperbilirubinemia with NB leads to damage to a variety of organs and systems (brain, liver, kidneys, lungs, heart, etc.), damage to the nuclei of the base of the brain is of leading clinical importance. The staining of the basal ganglia, globus pallidus, caudal nuclei, putamen of the lenticular nucleus is maximally expressed; less often the hippocampal gyrus, cerebellar tonsils, some nuclei of the thalamus optic, olives, dentate nucleus, etc. can be changed; this condition, according to the proposal of G. Schmorl (1904), was called “kernicterus”.

Clinical picture.

Edema form- the most severe manifestation of Rh-HDN. Typical is a burdened medical history of the mother - the birth of previous children in a family with HDN, miscarriages, stillbirths, prematurity, transfusions of Rh-incompatible blood, repeated abortions. During an ultrasound examination of the fetus, the Buddha pose is characteristic - the head is at the top, the lower limbs are bent in a position due to the barrel-shaped enlargement of the abdomen. knee joints, located unusually far from the body; "halo" around the cranial vault. Due to edema, the weight of the placenta is significantly increased. Normally, the weight of the placenta is 1/6-1/7 of the body weight of the fetus, but in the edematous form this ratio reaches 1:3 and even 1:1. The placental villi are enlarged, but their capillaries are morphologically immature and abnormal. Polyhydroamnion is characteristic. As a rule, mothers suffer from severe gestosis in the form of preeclampsia and eclampsia. Already at birth, the child has: severe pallor (rarely with an icteric tint) and general swelling, especially pronounced on the external genitalia, legs, head, face; a sharply increased barrel-shaped belly; significant hepato- and splenomegaly (a consequence of erythroid metaplasia in organs and severe fibrosis in the liver); expansion of the boundaries of relative cardiac dullness, muffling of heart sounds. Ascites is usually significant even in the absence of general fetal edema. The absence of jaundice at birth is associated with the release of fetal NP through the placenta. Very often, immediately after birth, respiratory disorders develop due to hypoplastic lungs or hyaline membrane disease. The cause of pulmonary hypoplasia is seen in an elevated diaphragm with hepatosplenomegaly and ascites. Hemorrhagic syndrome (hemorrhages in the brain, lungs, gastrointestinal tract) is common in children with the edematous form of tension-type headache. A minority of these children have decompensated DIC syndrome, but all have very low levels of procoagulants in the blood plasma, the synthesis of which is carried out in the liver. Characteristic: hypoproteinemia (serum protein level falls below 40-45 g/l), increased levels of BDG in the umbilical cord blood (and not just NB), severe anemia (hemoglobin concentration less than 100 g/l), normoblastosis and erythroblastosis of varying severity, thrombocytopenia. Anemia in such children can be so severe that, in combination with hypoproteinemia and damage to the vascular wall, it can lead to heart failure. Children with congenital edematous form of HDN who survive after active treatment (about half of these children die in the first days of life) often develop severe neonatal infections, liver cirrhosis, and encephalopathy.

Jaundice form- the most common form of HDN. At birth, the amniotic fluid, umbilical cord membranes, and primordial lubricant may be jaundiced. Characteristic is the early development of jaundice, which is noticed either at birth or within 24-36 hours of a newborn’s life. The earlier the jaundice appeared, the more severe the course of HDN is usually. Jaundice is predominantly warm yellow in color. The intensity and shade of the jaundiced color gradually change: first an orange tint, then bronze, then lemon and, finally, the color of an unripe lemon. Also characterized by an enlarged liver and spleen, icteric staining of the sclera and mucous membranes, and pasty abdomen is often observed. As the level of BN in the blood increases, children become lethargic, adynamic, suck poorly, their physiological reflexes for newborns decrease, and other signs of bilirubin intoxication appear. Blood tests reveal varying degrees of anemia, pseudoleukocytosis due to an increase in the number of normoblasts and erythroblasts, often thrombocytopenia, less often leukemoid reaction. The number of reticulocytes is also significantly increased (more than 5%).

If treatment is not started in a timely manner or is inadequate, the icteric form of HDN may be complicated by bilirubin encephalopathy and bile thickening syndrome. Bile thickening syndrome is diagnosed when jaundice acquires a greenish tint, the liver increases in size compared to previous examinations, and the intensity of urine color increases.

Bilirubin encephalopathy(BE) is rarely clinically detected in the first 36 hours of life, and usually its first manifestations are diagnosed on the 3-6th day of life. The first signs of BE are manifestations of bilirubin intoxication - lethargy, decreased muscle tone and appetite up to refusal of food, monotonous, unemotional cry, rapid depletion of physiological reflexes, regurgitation, vomiting. Then the classic signs of kernicterus appear - spasticity, stiff neck, forced body position with opisthotonus, stiff limbs and clenched hands; periodic excitement and a sharp “cerebral” high-frequency cry, bulging of a large fontanel, twitching of facial muscles or complete amymia, large-scale tremors of the hands, convulsions; "setting sun" symptom; disappearance of the Moro reflex and the visible reaction to a strong sound, the sucking reflex; nystagmus, Graefe's symptom; respiratory arrest, bradycardia, lethargy. The outcome of BE will be athetosis, choreoathetosis, paralysis, paresis; deafness; cerebral palsy; impaired mental function; dysarthria, etc.

Risk factors for bilirubin encephalopathy are hypoxia, severe asphyxia (especially complicated by severe hypercapnia), prematurity, hypo- or hyperglycemia, acidosis, hemorrhages in the brain and its membranes, convulsions, neuroinfections, hypothermia, fasting, hypoalbuminemia, certain medications (sulfonamides, alcohol, furosemide , diphenin, diazepam, indomethacin and salicylates, methicillin, oxacillin, cephalothin, cefoperazone).

Anemic form diagnosed in 10-20% of patients. Children are pale, somewhat lethargic, suck poorly and gain weight. They have an increase in the size of the liver and spleen, in the peripheral blood - anemia of varying severity in combination with normoblastosis, reticulocytosis, spherocytosis (with ABO conflict). Sometimes hypogenerator anemia is observed, i.e. there is no reticulocytosis and normoblastosis, which is explained by inhibition of bone marrow function and delayed release of immature and mature forms of red blood cells from it. NB levels are usually normal or moderately elevated. Signs of anemia appear at the end of the first or even the second week of life.

Diagnostics.

The studies required to diagnose tension-type headache are presented in Table 3.

Table 3.

Examination of the pregnant woman and fetus in case of suspected

hemolytic disease of the fetus.

All women with Rh-negative blood are tested at least three times for the titer of anti-Rhesus antibodies. The first study is carried out upon registration at the antenatal clinic. It is optimal to further conduct a repeat study at 18-20 weeks, and in the third trimester of pregnancy, carry it out every 4 weeks. The mother's Rh antibody test does not accurately predict the future severity of HDN in the child, and determining the level of bilirubin in the amniotic fluid is of great value. If the titer of Rh antibodies is 1:16-1:32 or greater, then at 6-28 weeks. amniocentesis is performed and the concentration of bilirubin-like substances in the amniotic fluid is determined. If the optical density with a 450 mm filter is more than 0.18, intrauterine blood transfusion is usually necessary. It is not performed on fetuses older than 32 weeks. gestation. Another method for diagnosing the congenital edematous form of HDN is ultrasound examination, which reveals fetal edema. It develops when the hemoglobin level is 70-100 g/l.

Since the prognosis for HDN depends on the content of hemoglobin and the concentration of bilirubin in the blood serum, it is first necessary to determine these indicators for the development of further medical tactics, and then conduct an examination to identify the causes of anemia and hyperbilirubinemia.

Examination plan for suspected TTH:

1. Determination of the blood group and Rhesus status of the mother and child.

2. Analysis of the child’s peripheral blood with evaluation of the blood smear.

3. Blood test with reticulocyte count.

4. Dynamic determination of bilirubin concentration in blood serum

see the child.

5. Immunological studies.

Immunological studies. In all children of Rh-negative mothers, the blood type and Rh affiliation, and serum bilirubin level are determined in the umbilical cord blood. In case of Rh incompatibility, the titer of Rh antibodies in the mother’s blood and milk is determined, and a direct Coombs reaction (preferably an aggregate agglutination test according to L.I. Idelson) is performed with the child’s red blood cells and an indirect Coombs reaction with the mother’s blood serum, and the dynamics of Rh is analyzed. antibodies in the mother's blood during pregnancy and the outcome of previous pregnancies. In case of ABO incompatibility, the titer of allohemagglutinins (to the erythrocyte antigen present in the child and absent in the mother) is determined in the blood and milk of the mother, in protein (colloid) and salt media, in order to distinguish natural agglutinins (have a large molecular weight and belong to class M immunoglobulins, do not penetrate the placenta) from immune ones (have a small molecular weight, belong to class G immunoglobulins, easily penetrate the placenta, and after birth - with milk, i.e. are responsible for the development of HDN). In the presence of immune antibodies, the titer of allohemagglutinins in the protein medium is two steps or more (i.e., 4 times or more) higher than in the saline medium. A direct Coombs test for ABO conflict in a child is usually weakly positive, i.e. slight agglutination appears after 4-8 minutes, whereas with Rh-conflict, pronounced agglutination is noticeable after 1 minute. If there is a conflict between the child and the mother regarding other rare erythrocyte antigenic factors (according to various authors, the frequency of such conflict ranges from 2 to 20% of all cases of HDN), the direct Coombs test is usually positive in the child and the indirect test in the mother, and incompatibility of the child’s erythrocytes and mother's serum in an individual compatibility test.

Changes in the child’s peripheral blood: anemia, hyperreticulocytosis, when viewing a blood smear - an excessive number of spherocytes (+++, +++++), pseudoleukocytosis due to an increased amount of nuclear forms of the erythroid series in the blood.

The plan for further laboratory examination of the child includes regular determinations of the level of glycemia (at least 4 times a day in the first 3-4 days of life), NB (at least 2-3 times a day until the level of NB in ​​the blood begins to decrease), plasma hemoglobin (in the first day and further as indicated), platelet count, transaminase activity (at least once) and other studies depending on the characteristics of the clinical picture.

Table 4.

Examinations for suspected HDN.

Diagnostic criteria for tension-type headache:

Clinical criteria:

*Dynamics of jaundice

Appears in the first 24 hours after birth (usually the first 12 hours);

Increases during the first 3-5 days of life;

Begins to fade from the end of the first to the beginning of the second week of life;

Disappears by the end of the third week of life.

*Features of the clinical picture

The skin with an AB0 conflict is usually bright yellow; with an Rh conflict it may have a lemon tint (jaundice on a pale background),

The general condition of the child depends on the severity of hemolysis and the degree of hyperbilirubinemia (from satisfactory to severe)

In the first hours and days of life, as a rule, there is an increase in the size of the liver and spleen;

Usually - normal coloring of stool and urine; against the background of phototherapy, there may be a green coloration of the stool and short-term darkening of the urine.

Laboratory criteria:

Concentration of bilirubin in umbilical cord blood (moment of birth) - in mild forms of immunological conflict for Rh and in all cases of A0 incompatibility -<=51 мкмоль/л; при тяжелых формах иммунологического конфликта по Rh и редким факторам – существенно выше 51 мкмоль/л;

The concentration of hemoglobin in umbilical cord blood in mild cases is at the lower limit of normal, in severe cases it is significantly reduced;

The hourly increase in bilirubin in the first day of life is more than 5.1 µmol/l/hour, in severe cases – more than 8.5 µmol/l/hour;

The maximum concentration of total bilirubin on days 3-4 in the peripheral or venous blood: >>256 µmol/l in full-term, >>171 µmol/l in premature;

Total blood bilirubin increases mainly due to the indirect fraction,

The relative proportion of the direct fraction is less than 20%;

decrease in hemoglobin level, red blood cell count and increase in reticulocyte count in clinical blood tests during the 1st week of life.

Based on clinical and laboratory data, three degrees of severity are distinguished:

a) A mild form of hemolytic disease (1st degree of severity) is characterized by some pallor of the skin, a slight decrease in the concentration of hemoglobin in the umbilical cord blood (up to 150 g/l), a moderate increase in bilirubin in the umbilical cord blood (up to 85.5 µmol/l), hourly an increase in bilirubin to 4-5 µmol/l, a moderate enlargement of the liver and spleen of less than 2.5 and 1 cm, respectively, a slight pastiness of the subcutaneous fat.

b) Moderate form (2nd degree of severity) is characterized by pallor of the skin, a decrease in cord blood hemoglobin in the range of 150-110 g/l, an increase in bilirubin in the range of 85.6-136.8 µmol/l, an hourly increase in bilirubin up to 6- 10 µmol/l, pasty subcutaneous fat, enlarged liver by 2.5 - 3.0 cm and spleen by 1.0 - 1.5 cm.

c) Severe form (3rd degree of severity) is characterized by severe pallor of the skin, a significant decrease in hemoglobin (less than 110 g/l), a significant increase in bilirubin in the umbilical cord blood (136.9 μmol/l or more), generalized edema, the presence of symptoms bilirubin damage to the brain of any severity and during all periods of the disease, respiratory and cardiac dysfunction in the absence of data indicating concomitant pneumo- or cardiopathy.

Differential diagnosis of tension-type headache carried out with hereditary hemolytic anemias (spherocytosis, elliptocytosis, stomatocytosis, deficiencies of certain erythrocyte enzymes, abnormalities of hemoglobin synthesis), which are characterized by a delayed (after 24 hours of life) appearance of the above clinical and laboratory signs, as well as changes in the shape and size of erythrocytes during a morphological examination of a blood smear, a violation of their osmotic stability in dynamics, changes in the activity of erythrocyte enzymes and the type of hemoglobin.

Examples of diagnosis formulation.

Hemolytic disease due to Rh conflict, edematous-icteric form, severe, complicated by bile thickening syndrome.

Hemolytic disease due to conflict according to the ABO system, icteric form, moderate severity, uncomplicated.

Modern principles of prevention and treatment.

Treatment of hemolytic disease of the fetus is carried out with Rh isoimmunization during the period of fetal development in order to correct anemia in the fetus, prevent massive hemolysis, and maintain pregnancy until the fetus reaches viability. Plasmapheresis and cordocentesis are used with intrauterine transfusion of red blood cells ("washed" red blood cells of blood group 0(II), Rh-negative are used).

Management tactics for tension headaches.

An important condition for the prevention and treatment of hyperbilirubinemia in newborns is the creation of optimal conditions for the early neonatal adaptation of the child. In all cases of illness in a newborn, care must be taken to maintain optimal body temperature, provide his body with a sufficient amount of fluid and nutrients, and prevent metabolic disorders such as hypoglycemia, hypoalbuminemia, hypoxemia and acidosis.

In cases where there are clinical signs of a severe form of hemolytic disease at the time of birth of a child in a woman with Rh-negative blood (severe pallor of the skin, icteric staining of the skin of the abdomen and umbilical cord, swelling of the soft tissues, enlargement of the liver and spleen), emergency PCD surgery is indicated without waiting for laboratory tests. data. (In this case, the partial PCD technique is used, in which 45-90 ml/kg of the child’s blood is replaced with a similar volume of donor red blood cells of group 0(1), Rh-negative)

In other cases, the management tactics for such children depend on the results of the initial laboratory examination and dynamic observation.

In order to prevent PCD in newborns with isoimmune HDN for any of the blood factors (Coombs test - positive), who have an hourly increase in bilirubin of more than 6.8 μmol/l/hour, despite phototherapy, it is advisable to prescribe standard immunoglobulins for intravenous administration. Human immunoglobulin preparations are administered intravenously to newborns with HDN slowly (over 2 hours) at a dose of 0.5-1.0 g/kg (on average 800 mg/kg) in the first hours after birth. If necessary, repeated administration is carried out 12 hours from the previous one.

The management tactics for children with tension-type headache over 24 hours of age depend on the absolute values ​​of bilirubin or the dynamics of these indicators. It is necessary to assess the intensity of jaundice with a description of the number of skin areas stained with bilirubin.

It should be remembered that there is a relative correspondence between the visual assessment of jaundice and the concentration of bilirubin: the larger the surface of the skin is yellow, the higher the level of total bilirubin in the blood: Staining of the 3rd zone in premature infants and the 4th zone in full-term newborns require urgent determination concentrations of total blood bilirubin for further management of children.

Scale of indications for exchange blood transfusion (N.P. Shabalov, I.A. Leshkevich).

The ordinate is the concentration of bilirubin in the blood serum (in µmol/l); on the x-axis - the child’s age in hours; dotted line - bilirubin concentrations at which PCA is necessary in children with no risk factors for bilirubin encephalopathy; solid lines - bilirubin concentrations at which BPC is necessary in children with the presence of risk factors for bilirubin encephalopathy (with ABO and Rh conflict, respectively)