Hemolytic disease. Symptoms, clinical picture, treatment. What is HDN (hemolytic disease of the newborn), causes and treatment What is hemolytic disease of the newborn

erythroblastosis fetalis

Hemolytic disease of the newborn occurs when a child inherits an Rh factor or blood type from the father that is incompatible with the mother's blood. The conflict leads to massive breakdown of red blood cells and severe complications, including the death of the body over the next few hours/days. But it is now possible to treat hemolytic disease of newborns, as well as prevent it. In the ICD-10 system, this disease is assigned code P55.

The etiology (cause) of the phenomenon in which antibodies incompatible with its blood from the mother’s body enter the fetal blood lies in heredity and its laws. But sometimes episodes from her past can also lead to the appearance of such proteins in a mother, for example, if she has a history of repeated blood transfusions. Or if the blood was transfused once, but it did not suit her well (say, it was selected without taking into account Rh). Such risk factors are rarely taken into account by parents, as is the compatibility of their blood groups. Meanwhile, they can create situations where the family already has a child, and everything is fine with him, and the second suddenly starts a pathological process.

When can pathology occur?

The causes of hemolytic disease of newborns can be different, and it is not always a matter of the laws of genetics. So, its appearance can be expected in the following cases.

• If the mother is Rh negative and the child is positive. The Rh factor (special blood proteins inherited from our tailed ancestors) is either present in the blood or it is not. It tends to be inherited. This means that if at least one of the grandparents has it, the child can inherit Rh positive from them, even if both of his parents are Rh negative. Thus, the greatest danger to the unborn fetus is the Rh-negative mother. After all, the likelihood that Rh positive will be passed on to her baby from one of her ancestors is much higher than the likelihood that this will not happen.
• If there is a blood type conflict. Now medicine distinguishes not three, but four blood groups, where the fourth has simultaneously the characteristics of the third and second groups. The domestic labeling system designates them in Latin numerals. And in Western and American medicine the so-called AB0 system. In it, group I is designated as zero, group II is designated by the letter “A”, and group III is designated by the letter “B”. Group IV, as representing a “hybrid” of groups II and III, is designated as “AB”. The mechanism of development or pathogenesis of hemolytic disease according to the blood group of newborns lies in the incompatibility of certain proteins characteristic of a particular group. Of these combinations, group 0 (that is, I) is in the mother versus group A or B (II or III) in the child.
• If you have acquired hypersensitivity in the past. That is, blood with the opposite rhesus entered the mother’s body and the corresponding antibodies were formed. This could occur during donor blood transfusion; abortion or miscarriage (blood may be mixed); amniotic fluid/chorionic villus biopsy.

Only a blood test can determine the blood type and Rh factor in the mother and fetus, as well as answer the question of whether the mother has Rh antibodies. All these processes, including the production of antibodies to the blood of another group, are asymptomatic, the mother does not subjectively feel them, and therefore does not experience anxiety.

Manifestations of different forms of hemolytic disease of newborns

This conflict of blood cells between a mother and her baby also has another name - erythroblastosis fetalis. But in reality, this term reflects one of the consequences of the massive destruction of red blood cells. It means that the patient’s blood contains large number immature red blood cells - the result of increased activity bone marrow who is in a hurry to replace adults dying under the influence of any factors blood cells. These immature red blood cells are called reticulocytes. Erythroblastosis occurs in all cases of massive breakdown of red blood cells, regardless of its cause.

And in the classification of hemolytic disease, three main forms of the course are distinguished. Not only the picture of her symptoms, but also the prognosis for the child’s survival/recovery depends on them.

• Edema form. Fortunately, it is the rarest, occurring during the gestation period. 99% of children suffering from it die before birth or soon after it, since their condition at the time of birth is extremely severe, and it is almost impossible to independently supply tissues with oxygen. The newborn has large-scale edema, the liver is sharply enlarged, reflexes are almost absent, and there is heart failure (in addition to respiratory failure). The onset of hemolytic disease in early pregnancy often ends in miscarriage.
• Jaundice form. It is more widespread than others and manifests itself within the next 24 hours after birth, since “incest” here occurs only during childbirth. It can also be very difficult and end in death, but in most cases this scenario can be avoided. Jaundice and anemia may persist in the child for several months.
• Anemic form. It also occurs during the first days or 2-3 weeks after birth. In general, with it, the newborn behaves almost like a healthy child. The only symptoms that may be observed are some lethargy, pallor, an enlarged liver and spleen, and decreased appetite. Timely treatment can shorten the entire period of anemic hemolytic disease to a month.

Edema

The most dangerous form Hemolytic disease of the newborn begins during pregnancy, so early signs can be detected in the mother rather than in the fetus.

• At mom's. The level of bilirubin in the blood increases. Bilirubin is a brown organic dye that gives the characteristic color to bile, stool and urine. It is formed when the liver processes old red blood cells. And even more precisely, with the breakdown of the red glandular protein hemoglobin in their composition. An increase in the concentration of bilirubin in the blood colors yellow all tissues, including oral mucous membranes and eyeballs. This phenomenon is called jaundice, and it indicates the accelerated destruction of red blood cells directly in the bloodstream, so large-scale that the liver simply does not have time to filter out all the bilirubin released.
• In the fetus. A huge belly and tissue swelling are recorded. A CT scanner is usually more useful than an ultrasound machine for detecting such signs. They are deliberately sought for when hemolytic disease is suspected. For example, if the concentration of bilirubin in the mother’s blood increases or her blood is sensitized by the Rh factor. In addition, increased monitoring is required in cases where the chances of incompatibility of the blood group or Rhesus of the fetus and mother are very high.

After birth, diagnosing hemolytic disease in a newborn child in its edematous form is not difficult, since it is clearly indicated by:

• huge belly;
• signs of oxygen starvation;
• large-scale swelling throughout the body;
• pallor of the skin and mucous membranes;
• flaccid muscle tone;
• decreased reflexes;
• pulmonary and heart failure;
• critically low performance blood hemoglobin.

Jaundice

The main symptom of the icteric form is indicated in its name. True, in this case, a differential diagnosis of hemolytic disease of newborns with other pathologies accompanied by jaundice is necessary: viral hepatitis, malaria, bone marrow/blood/liver cancer. And in addition to jaundice, it manifests itself in three groups of symptoms.

1. Enlarged liver and spleen. This happens in the first two to three days after birth.
2. Drowsiness, lethargy of behavior and reflexes. These are signs of brain hypoxia, associated with the inability of the blood to provide it with oxygen due to a reduction in the number of “functional” red blood cells in the blood.
3. Discoloration of stool. It occurs against the background of darkening of urine, gases and regurgitation after eating. All these signs are explained by cholestasis - retention of bile in gallbladder(in this case, due to its thickening with excess bilirubin).

The severe course of the icteric form may also be accompanied by bulging fontanelles on the newborn’s skull, convulsions, throwing the head up and a “brain” cry - monotonous, piercing and continuous. Such signs indicate the onset of so-called bilirubin encephalopathy (kernicterus, as it affects the nuclei of the brain).

The essence of this process lies in the toxic effect of free bilirubin on cortical cells, since this substance can penetrate the blood-brain barrier (the brain’s own protective system against foreign components carried by the bloodstream). A child in such a state may stop breathing, lose facial expressions, and develop a sharp reaction to even the weakest stimuli.

Anemic

This form is manifested only by a slight enlargement of the liver and spleen, moderate hypoxia (lack of oxygen), which forces the baby to move less and sleep more often. His skin may be paler than usual, but this symptom is also erased.

Hemolytic disease of the newborn has one interesting feature. The fact is that when mother and child are incompatible only by the Rh factor, it is usually more severe than when there is incompatibility only by blood type or by both indicators at the same time. Moreover, if the conflict comes down to different rhesuses, in the case of one pregnancy it may appear, but not with the next, and vice versa. But a blood type conflict always manifests itself immediately and cannot be corrected in the future.

Therapy

The basic principle of treatment for hemolytic disease of the newborn is to completely replace the child’s own blood with donor blood. It is carried out if the disease has occurred, progresses and threatens his life. Donor blood transfusion can be performed:

• before birth (via the umbilical vein),
• after the birth of the child.

Blood has to be transfused that is identical both in group (a compatible group will not work here - you need the same one as the child had) and in Rhesus. This means that while the fetus is in the womb, the mother’s body will continue to fight new blood cells just as actively as it did with the old ones.

Emergency care for a baby who is born with signs of hemolytic disease should be provided within the next few hours. It usually involves a combination of blood transfusion followed by stimulation of the heart and lungs. In the future, the baby only needs:

• standard nursing care;
• presence of mother;
• a few more blood biochemistry tests.

Biochemistry is done at intervals of 7-15 days, but it is needed to track changes indicating rejection of donor blood for other reasons that are no longer related to hemolytic disease.

Treatment with traditional medicine

Treatment of hemolytic disease in newborns with alternative medicine methods is unacceptable and directly threatens their lives.

• Homeopathy. It is not popular even among healers, since we are talking not about folk, but about the author’s technique. And reviews about it from scientists are also negative.
• Herbal treatment. In this case, it is acceptable in theory (say, a course of choleretic drugs like corn silk). But in practice, it can make a child allergic for life, since all plants are allergens. Meanwhile, the baby’s immune defense has not yet learned how to work properly. Plus, she had only recently been in a situation where she was either suppressed by her mother’s immunity, or she herself had to deal with completely new blood and foreign antibodies in its composition.

Therefore, only non-toxic (!) medicinal plants. Their course can be carried out no earlier than a month after the disappearance of all symptoms of the disease, and it should not last more than a week. Herbs should be used at a minimum - one or two, and it is better to avoid making multi-component mixtures.

Prevention

Prevention of hemolytic disease in infants involves preventing the formation of Rh antibodies in the mother before and during pregnancy. Such activities are carried out if it is not available at the time of the start of the procedure, since, in otherwise, proactive measures will no longer work.

In other words, the prevention of such conflicts begins and ends with the mother’s body. The only way to avoid them if there is a discrepancy between the baby's Rh and/or blood type is to timely administer anti-Rhesus immunoglobulin to her.

The point of the procedure is that immunoglobulins capture Rh proteins from the blood of a “positive” baby, without letting them pass into the “negative” blood. circulatory system moms. If there is no mixing of blood different types, antibodies to the baby’s blood will not form in the mother’s blood.

Long-term consequences

The immediate complications of hemolytic disease in a newborn child largely coincide with its symptoms. These include liver/gallbladder diseases, developmental delays, and cardiovascular pathologies. And in the future, there may be consequences of hemolytic disease of newborns associated with the effects of red blood cell destruction products (billirubin) on the brain:

• Cerebral palsy (cerebral palsy);
• deafness, blindness and other sensory impairments;
• developmental delay and decreased intelligence;
• epilepsy.

The basis of the metabolic system is blood circulation and the work of filtering organs - the liver, spleen and kidneys. Hemolytic disease of newborns can cause serious complications on them. If they exist, in the future you need to beware of any prescriptions for your child (medical and folk) medicines. Therefore, children who have had it are prohibited from most standard childhood vaccinations, including the so-called. BCG (vaccination against tuberculosis). They should be avoided for at least three months after treatment.

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Six out of a thousand children are diagnosed with hemolytic disease of the newborn(GBN). This is a consequence of an immunological conflict (incompatibility) between the blood of a mother and her child. Who gets it? How does this disease progress and how dangerous is it? Is there effective ways helping kids?

Why does hemolytic disease of the newborn occur?

This is all due to differences in the antigen (genetic) composition of proteins in red blood cells - erythrocytes. Today, doctors already know 14 group systems, which include about 100 antigens located on the membranes of red blood cells. The child receives some of them from the mother, the other from the father. And if the mother does not have such proteins in her blood, but the fetus does, HDN develops.

The most famous systems are Rhesus and ABO. But other antigens, previously considered a rare cause of tension-type headache, are causing it more and more every day. That is, hemolytic disease of newborns can arise not only due to Rh conflict or incompatibility in blood groups (in the ABO system), but also due to differences in any of the 12 other group systems.

The mechanism for the development of an immunological conflict in case of incompatibility for each of the 14 systems is approximately the same. After the 8th week of pregnancy (usually in the second half), a tiny amount of fetal blood (that is, antigens) penetrates the placenta into the mother’s bloodstream. In response, her immune system produces cells - antibodies that destroy strangers. But they are not released once, but, like border guards, constantly circulate in the bloodstream, ready for a repeated attack. Getting to the fetus in utero, during childbirth or with mother's milk, they cause destruction (hemolysis) of its red blood cells. That is, the “battle” of maternal antibodies against the child’s red blood cells already occurs in the baby’s body. Its duration and aggressiveness depends on the number of immune cells that have penetrated and the maturity of the child. This is hemolytic disease.

The most dangerous type of immunological conflict is blood incompatibility according to the Rh system. In 90% of cases, it occurs in an Rh-negative mother who has already given birth to an Rh-positive child. That is, the first pregnancy, as a rule, proceeds without HDN. The second Rh-positive fetus begins to suffer in utero, since the woman's immune system already has memory cells that quickly activate and multiply to destroy the baby's red blood cells. Therefore, even before birth, the baby’s health may suffer greatly, even to the point of antenatal death. And after childbirth, the disease develops from the first minutes, pathological symptoms are growing very rapidly.

If the blood of the fetus and its mother is incompatible according to the ABO system, hemolytic disease of the newborn develops already during the first pregnancy. But clinically it is rarely as severe as with Rh conflict. This is due to the fact that some tissues of the baby, the fetal membranes and the umbilical cord, have a similar antigenic set and take part of the impact of the maternal killer cells. That is, the disease, if adequately treated, proceeds much milder, without catastrophic consequences.

When registering a woman for pregnancy, she will be required to check not only her blood type, but also the father of the child. The risk of developing TTH will be:

• for mothers with O(1) group, if the spouse has any other;
• in women with A (2) group, if the husband has B (3) or AB (4);
• for mothers with B (3) group, if the child’s father has A (2) or AB (4).

Clinical forms of hemolytic disease of newborns

1. Anemic.

Due to the destruction of red blood cells in a child, their number and hemoglobin content in the blood gradually decrease. A general blood test at the beginning of a conflict reveals increased amount young forms of red blood cells - reticulocytes, and after a few days - their disappearance due to depletion of bone marrow reserves. This form of HDN develops in mild conflicts in the ABO system and in other rare antigenic groups (for example, Kell, S, Kidd, M, Lutheran). Due to oxygen deficiency, the child is pale, lethargic, with an enlarged liver. He sucks weakly and is slowly gaining weight. Treatment may require the introduction of donor red blood cells. Anemia accompanies the baby for several months; hemoglobin may drop sharply again after about 3 weeks. Therefore, such children need to be repeated repeatedly general analysis blood so as not to miss the worsening of the disease. Remember that severe anemia leaves a negative imprint on the further intellectual development of the baby!

2. Jaundice.

The most common variant of the course of hemolytic disease. Even in full-term newborns, the activity of liver enzyme systems “starts” a few days after birth. The shorter the gestational age, the more pronounced the immaturity of the liver, and the more longer blood The baby is poorly cleared of bilirubin released during the breakdown of red blood cells. As a result, it accumulates, causing icteric discoloration of the skin and all mucous membranes. In addition, it is deposited in the form of crystals in the kidney tubules, damaging them, causing damage to the pancreas and intestinal walls.

The most dangerous complication of hyperbilirubinemia is kernicterus. This is toxic damage to the nuclei of the brain, reversible only in initial stage. Next comes their death, manifested by convulsions, impaired consciousness up to coma. Surviving children are left with persistent neurological and mental defects and often develop cerebral palsy.

A blood test, along with signs of anemia, reveals an increase in indirect, and then direct, bilirubin. Its critical level, at which symptoms of kernicterus appear, is different for each child. It is influenced by gestational age, the presence of concomitant infection, the consequences of intrauterine and postpartum oxygen starvation, hypothermia, and fasting. For full-term babies, the approximate figure is about 400 µmol/l.

3. Edema.

4. Intrauterine death with maceration.

This is the death of the fetus in the early stages of gestation against the background of the catastrophic development of the edematous form of hemolytic disease.

Complications of hemolytic disease of the newborn

Long-term persistence of anemia impairs the physical and intellectual development of the child. Low hemoglobin is not just about pale skin. Red blood cells bring oxygen to every cell of the body, without which a person cannot exist. With its deficiency (hypoxia), all life processes first slow down and then stop altogether. The lower the hemoglobin, the more the baby suffers: his heart, skin, lungs, intestines, all endocrine organs and the brain.

Complications of jaundice, in addition to those listed above, may be bile thickening syndrome and associated digestive disorders, abdominal cramps and changes in blood tests. Even with mild form bilirubin encephalopathy, brain damage can cause prolonged disruption of sleep and wakefulness, increased breathing or heart rate, slower mental development, asthenic syndrome, neuroses and headaches.

It has been noted that after HDN, children under 2 years of age are more susceptible to infectious diseases, take longer to recover and more often require more active treatment, including appointments antibacterial drugs. This indicates the adverse effect of high concentrations of bilirubin on the child’s immune system.

Treatment of hemolytic disease of newborns

If an increase in the titer of anti-Rhesus antibodies is detected during pregnancy, the following treatment methods for women are used to prevent severe forms of HDN:

1. Plasmapheresis.

Starting from the 16th week, 2 – 3 times with an interval of 4 to 8 weeks, the mother’s plasma is removed along with the accumulated aggressive immune cells.

2. Grafting a skin flap from the child’s father.

This foreign graft measuring 2 by 2 cm takes on the blow of anti-Rhesus antibodies, saving the child’s red blood cells from hemolysis.

3. Intrauterine replacement blood transfusion using cordocentesis.

For any type of HDN the following are used:

1. Regular courses of nonspecific therapy aimed at reducing oxygen starvation of the fetus. These are vitamins, antihypoxic drugs, antianemic drugs, oxygen therapy, including hyperbaric oxygenation.
2. Stimulating the maturation of liver enzyme systems by taking phenobarbital 3 days before the planned delivery.
3. Attempts are being made to use a kind of intrauterine phototherapy: laser beams with a certain wavelength to convert the toxic form of bilirubin into one that is safe for the fetus.

After birth volume medical care directly depends on the severity and speed of development of symptoms of hemolytic disease. Complex treatment may include:

• prevention of bile thickening syndrome and stagnation of intestinal contents (cleansing enemas, early start of feeding and mandatory supplementation);
• activation of liver enzymes that neutralize indirect bilirubin (phenobarbital);
• administration of intravenous glucose solution to prevent kidney damage and increase the excretion of the water-soluble fraction of bilirubin in the urine;
• phototherapy: long-term irradiation of a child using lamps of a certain wavelength spectrum to convert harmful bilirubin accumulated in the skin into harmless;
• replacement blood transfusion - for icteric and edematous forms of HDN, red blood cell transfusion - for anemic.

Today doctors have real opportunity help a woman bear and give birth to a healthy child if their blood is immunologically incompatible. It is only important that the expectant mother actively cooperates with doctors and follows all their recommendations.

– intrauterine immunological conflict caused by the incompatibility of the blood of the fetus and mother for a number of antigens, which leads to hemolysis of the child’s red blood cells under the influence of maternal antibodies that overcome the placental barrier. Hemolytic disease of the fetus can occur in an edematous, icteric, anemic form and even lead to intrauterine fetal death. Diagnosis involves examining amniotic fluid (amniocentesis), umbilical cord blood, bilirubin and hemoglobin in the newborn. Treatment of hemolytic disease of the fetus requires phototherapy, intravenous infusion of solutions, and exchange blood transfusion.

General information

The pathogenetic basis of hemolytic disease consists of processes caused by immunological (antigen-antibody) incompatibility of the blood of the fetus and mother. In this case, the antigens present in the blood of the fetus are inherited from the father, but are absent in the blood of the mother. Most often (1 case in 250 pregnancies), hemolytic disease of the fetus develops due to a conflict over the Rh factor; can also occur with group incompatibility of blood and other less studied antigens. Hemolytic disease of the fetus leads to perinatal mortality in 3.5% of cases.

With hemolytic disease of the fetus, under the influence of maternal antibodies formed to fetal antigens and penetrating the placenta, the child develops hemolysis of red blood cells and inhibition of hemipoiesis. Toxic effects the breakdown products of red blood cells on the body of the fetus (newborn) leads to the development of anemia, an increase in bilirubin and blast (immature) red blood cells.

Causes of hemolytic disease of the fetus

An immunological conflict leading to hemolytic disease of the fetus most often develops with isoserological incompatibility of blood according to the Rhesus (Rh) system, when the mother has Rh-negative blood and the fetus has Rh-positive blood. In this case, it is called Rhesus conflict. Isoimmunization can occur in two ways: iatrogenic (when a woman is sensitized by Rh(+) blood transfusions in the past) or through fetal-maternal transplacental transfer of fetal red blood cells into the maternal bloodstream during pregnancy and childbirth. In the case of Rh incompatibility, hemolytic disease of the fetus is rarely associated with the first pregnancy; most often develops from the 2nd or 3rd pregnancy with an increase in risks with each subsequent gestation.

Another possible reason Hemoloitic disease is caused by the incompatibility of the blood of the fetus and mother according to the AB0 system, i.e., when the mother’s blood group is 0 (I), and the fetus has any other. In this case, antigens A and B from the fetus penetrate through the placenta into the maternal bloodstream and cause the production of immune α- and β-antibodies with subsequent antigen-antibody conflict. Fetal hemolytic disease with ABO incompatibility has a milder course than with Rh incompatibility. With AB0 incompatibility, hemolytic disease of the fetus can develop already during the first pregnancy.

In relatively rare cases, hemolytic disease of the fetus may be associated with immunological conflicts in the Duffy, Kell, MNSs, Kidd, Lutheran, etc. systems or antigens P, S, N, M.

Manifestations of hemolytic disease of the fetus

In pregnant women, no specific pattern of pathology is observed; sometimes an increase in intrauterine reactions can cause a woman to experience a symptom complex similar to preeclampsia. Hemolytic disease of the fetus can manifest itself in the following ways: intrauterine fetal death in the period from 20 to 30 weeks of pregnancy; edematous, icteric or anemic forms. General manifestations, characteristic of all forms of hemolytic disease of the fetus, are the presence of normochromic anemia with an increase in erythroblasts in the blood, hepatomegaly and splenomegaly.

With the edematous version of hemolytic disease in the fetus, the size of the spleen, liver, heart, and glands increases, and hypoalbuminemia increases. These changes are accompanied by pronounced swelling of the subcutaneous fat, ascites, pericarditis, pleurisy, and an increase in the child’s weight by 2 times compared to the norm. With the edematous variant of hemolytic disease of the fetus, pronounced anemia (Er -1-1.5 x 1012/l, Hb 35-50 g/l), erythroblastemia, enlargement and swelling of the placenta are observed. Severe metabolic disorders can cause intrauterine fetal death or the death of a child shortly after birth. The edematous form of hemolytic disease of the fetus is characterized by an extremely severe course, which in most cases leads to death.

With the icteric variant of hemolytic disease of the fetus, the child is more often born from urgent labor, full-term, often with normal skin color. In this case, hemolytic disease of the fetus manifests itself several hours after birth - the child’s skin becomes jaundiced; Less commonly, jaundice is congenital. In newborns with the icteric form of hemolytic disease, the spleen, liver, lymph nodes, and sometimes the heart are enlarged; direct bilirubin in the blood.

Hyperbilirubinemia is dangerous due to the possibility of damage to hepatocytes, cardiomyocytes, nephrons, and neurons with the development of bilirubin encephalopathy. With kernicterus (bilirubin intoxication), the child is lethargic, sucks poorly, often regurgitates, and develops hyporeflexia, vomiting, and convulsions. The critical level of indirect bilirubin, dangerous in terms of damage to the central nervous system, is more than 306-340 µmol/l in full-term infants and 170-204 µmol/l in premature infants. The consequence of bilirubin encephalopathy may be the death of the child or subsequent mental retardation.

In the anemic form of hemolytic disease, the damaging effect on the fetus is usually small. Anemia, pale skin, hepatomegaly and splenomegaly come to the fore. The severity of the manifestations of hemolytic disease of the fetus is determined by the antibody titer in the pregnant woman and the degree of maturity of the newborn: the disease is more severe in premature infants.

Diagnosis of hemolytic disease of the fetus

Considering that hemolytic disease is often accompanied by hypoxia, cardiotocography is performed to assess fetal cardiac activity. If evidence of hemolytic disease of the fetus is obtained, invasive studies are required - cordocentesis and amniocentesis under ultrasound guidance. At the birth of a child, its Rh and group affiliation are immediately determined, and the content of Hb and bilirubin in the umbilical cord blood is examined.

Treatment of hemolytic disease of the fetus

The therapeutic objectives for hemolytic disease of the fetus are the rapid removal of toxic factors of hemolysis from the child’s blood - indirect bilirubin and antibodies, as well as increasing the functions of the suffering systems and organs. The choice of method of delivery for women with isoimmunization is determined by the condition of the fetus, gestational age, and the preparedness of the birth canal. In the absence of data for a severe form of hemolytic disease of the fetus, at a gestational age of more than 36 weeks, natural birth is possible at cervical maturity. If the fetus is in serious condition, a caesarean section is preferable 2-3 weeks before the expected due date.

In newborns with hemolytic disease of the fetus, Hb, Ht, and bilirubin levels are monitored daily. If necessary, correction of anemia with red blood cells and infusion detoxification therapy are carried out. An important component of the treatment of hemolytic disease of the fetus is phototherapy, which promotes the destruction of indirect bilirubin in the child’s skin. Light therapy is carried out in pulsed or continuous mode using fluorescent or blue light lamps.

For more severe manifestations of hemolytic disease of the fetus, drip intragastric fluid administration and exchange blood transfusion are indicated. In case of hemolytic disease of the fetus caused by an Rh conflict, single-group Rh (-) blood is used for exchange transfusion. In case of ABO incompatibility, red blood cells of group 0(I) are transfused in accordance with the Rh affiliation of the newborn and plasma of the same group. The development of pulmonary edema and severe respiratory failure requires mechanical ventilation; the presence of ascites dictates the need to perform laparocentesis under ultrasound guidance.

Prevention of hemolytic disease of the fetus

It consists of preventing Rh immunization of women - careful blood transfusion taking into account Rh affiliation. Women with Rh(-) blood are categorically not recommended to terminate a pregnancy that has occurred for the first time. A method of specific prevention of Rh conflict in women with Rh(-) blood is the administration of human anti-Rhesus immunoglobulin Rho after abortion, birth of an Rh(+) fetus, ectopic pregnancy, as well as after invasive prenatal diagnosis - chorionic villus biopsy, amniocentesis, cordocentesis.

Hemolytic disease in newborns (HDN) is a pathology that occurs during fetal development or during the first hours after birth. The cause of this pathology is incompatibility between the blood of the fetus and its mother, when the woman begins to produce antibodies to the child’s red blood cells (immunological conflict). The development of the disease occurs due to the fact that antibodies from female body enter the child's body. In this way, active destruction of the baby’s red blood cells occurs... in addition, HDN is almost the first on the list of reasons that cause kernicterus in babies and anemia.

It is worth noting that in recent years Cases of hemolytic disease have increased significantly - approximately one case per 250-300 births. As a rule, this pathology occurs due to Rh conflict between a woman and a child. If we talk about blood group incompatibility, then there are several times fewer such cases. Incompatibility with other erythrocyte antigens is generally considered rare, because such cases are isolated.

If hemolytic disease develops according to the Rh factor, then in 3-6% of cases it proceeds quite mildly, but at the same time it is very difficult to diagnose. There are cases where hemolytic disease of this type was discovered in a newborn already in an advanced stage, when treatment does not bring tangible results.

When a newborn begins to develop hemolysis or destruction of red blood cells, the level of bilirubin in his blood very quickly increases and provokes the development of anemia. When the level of bilirubin is too high and exceeds a critical level, it begins to release toxins that affect the brain and many other organs of the child. In addition, anemia begins to progress very quickly and the body begins to do everything possible to compensate for the lack of oxygen. Thus, the liver begins to increase in size, followed by the spleen.

Clinical forms of hemolytic anemia in a newborn baby

1. Edematous form of HDN. This form is the most severe and begins to develop in utero. As a result of the destruction of red blood cells, the child develops a severe form of anemia, metabolism is disrupted, tissues swell and protein levels decrease. If HDN begins to develop on early pregnancy, it could end in miscarriage. If the child still survives, he will be born very pale, with pronounced swelling.
2. Jaundice form of HDN. This form can be found most often. The main symptoms are the early development of jaundice, anemia and a significant enlargement of the liver and spleen. Jaundice may appear immediately after birth or after about 1-2 days, which is not typical for physiological jaundice. The earlier it appears, the more severe HDN will be. Signs of the disease include greenish skin color, dark urine and colorless feces.
3. Anemic form of HDN. This form is the most gentle and easiest. It appears within seven days after the birth of the child. It is not always possible to immediately notice the appearance of pale skin, and therefore HDN can be diagnosed at 2-3 weeks of the baby’s life. Outwardly, the child remains the same, but the liver and spleen begin to increase in size. Bilirubin levels will be elevated, but only slightly. This form of the disease can be easily cured without harmful consequences for the baby's health.

Diagnosis and treatment of hemolytic disease of newborns

Antenatal diagnosis is carried out during pregnancy in women who are at risk. If a woman is Rh negative, she must be tested three times for the presence of antibodies in her blood. It is very important to take into account the results over time, because they can show a high risk of a child’s disease. In order to finally make sure of the diagnosis, you need to examine amniotic fluid for the presence of bilirubin, iron, glucose and protein levels. In addition, changes in fetal development, which can be detected by ultrasound, may cause suspicion.

Postnatal diagnosis is carried out after the birth of the child and consists entirely of studying clinical symptoms illnesses in a child. In this case, it is necessary to study absolutely all the data, both in complex and in dynamics.

How to treat hemolytic disease in a newborn baby

Indications for blood transfusion if the baby is premature

• The level of indirect bilirubin exceeds the critical value;
• bilirubin level increases every hour by approximately 6-10 µmol/l;
• a severe form of anemia is observed.

In addition, vitamins B2, B6, C can be used to treat hemolytic disease. activated carbon, prednisone, cocarboxylase or phenobarbital. It is worth noting that previously it was believed that if a child had a more hemolytic disease, then he should not be put to the breast. Today it has been proven that the antibodies that are in a woman’s milk do not enter the child’s blood and are completely destroyed under the influence of hydrochloric acid baby's stomach. Therefore, there is no need to be afraid of anything and put your baby to your breast as often as possible. This will help him get stronger faster and begin to fight the disease on his own.

Prevention of hemolytic disease in a newborn baby

One of the most severe childhood pathologies is hemolytic disease of newborns (HDN), which occurs when the immune systems of mother and child conflict, which is accompanied by massive destruction of red blood cells. Therefore, this disease of the fetus and newborn is also known as erystoblastosis - This is a sad result of the categorical differences in the blood of mother and baby according to the Rh or ABO system.

The main cause of erythroblastosis in an infant is the opposite difference in the blood of mother and baby, often in the Rh factor. More rarely, the culprits are blood group antigens (in the ABO system), and less often they encounter opposition of a different nature.

What is the predisposition to Rh conflict between mother and baby? When a mother with minus rhesus is pregnant with a baby with plus rhesus. Most often, this is why hemolytic disease of newborns manifests itself, starting development already in the womb.

The reason for the clash of immunities in the ABO system is a mismatch in blood groups: O(1) blood group in the mother and A(2) or B(3) in the fetus.

It is worth noting that a child is not always born sick. And only when the mother had previously experienced so-called sensitization, that is, increased sensitivity to foreign blood components that she encountered for one reason or another.

Maternal sensitization may have different sources. For example, a mother who is Rh negative becomes sensitized after receiving a transfusion of Rh positive blood (this could have happened a long time ago, even when she was a child). In addition, sensitization occurs during a miscarriage, and if there was an induced abortion. Also, the main culprits of maternal sensitization are childbirth. Therefore, with each subsequent child the risk increases.

If we are talking about immune incompatibility according to the ABO system, it does not matter what kind of pregnancy a woman has, since we are faced with sensitization to antigens every day - when eating, with vaccinations, during some infections.

In addition to the above-mentioned discrepancies in the Rh factor and the ABO system, the placenta occupies a special place, since it provides direct contact between the organisms of the mother and the baby when he is in the womb. When the barrier itself is broken, the exchange of antibodies and antigens in the bloodstreams of mother and baby occurs more easily.

During the prenatal period, hostile blood bodies penetrate inside along with red blood cells. These bodies (Rh factor, antigens A and B) promote the formation of antibodies in the blood, and they then penetrate the protective barrier into the bloodstream of the pregnant baby. The result of this exchange is the combination of antigens and antibodies, causing pathological destruction of red blood cells.

The consequences of such destruction with the participation of hostile bodies have a detrimental effect on the development of the fetus. One of the consequences of this breakdown is an increase in the concentration of toxic bilirubin and the development of anemia (anemia).

Bilirubin that has not passed through the liver is toxic to humans, and even more so to an infant. It has the ability to overcome the obstacle separating the circulatory system and the central nervous system, and also causes damage to the subcortical nuclei and cerebral cortex, which is the cause of “kernicterus.”

If it has developed, then as a result of the destruction of red blood cells, new blood cells are formed - erythroblasts. Therefore, this disease is also called erythroblastosis.

Forms

Depending on the type of immunological conflict, there are following forms

• Hemolytic disease of newborns due to Rh factor conflict;
• Hemolytic disease of newborns due to blood group conflict (ABO incompatibility);
• More rare forms (conflict with other antigenic systems).

Clinical forms:

• Edema;
• Jaundice;
• Anemic.

Based on severity, the following forms of the disease are distinguished:

• Mild: symptoms are moderate or there are only laboratory indicators.
• Moderate: bilirubin in the blood is increased, but intoxication and complications have not been identified. In the first 5–11 hours after the birth of the baby, it appears (depending on the Rh or ABO conflict), in the 1st hour of life it is less than 140 g/l, bilirubin in the blood from the umbilical cord exceeds 60 µmol/l, the liver and spleen are enlarged in size.
• Severe: edematous form of the disease, symptoms of kernicterus, respiratory and cardiac function disorders.

Symptoms

Clinical symptoms vary depending on one form or another of pathology: edematous, anemic or icteric.

Edema

The edematous form, similarly called hydrops fetalis, is the most rare, and exceeds all others in the severity of the disease. Here are its signs and symptoms:

• The beginning of development is intrauterine;
• High probability of miscarriage in the first trimester of pregnancy;
• Less commonly, later death of the fetus or birth in an aggravated position with edema characteristic of this form, a profound deficiency of hemoglobin and red blood cells in the bloodstream, with oxygen starvation and heart failure;
• Intense, almost waxy, paleness of the baby's skin;
• Sharp muscle strengthening, reflex inhibition;
• Large belly due to enlarged liver and spleen;
• Extensive tissue swelling.

Anemic

The anemic form is the mildest possible. Its symptoms:

• Can be recognized in the near future (up to four to five days) after the birth of the child;
• Anemia gradually develops, the skin and mucous membranes turn pale, the abdomen enlarges;
• In general, it does not greatly affect the child’s well-being.

Jaundice

The icteric form is the most common. Its symptoms:

• The tissues acquire a pronounced yellow tint due to the hyperaccumulation of bilirubin pigment and its derivatives in the bloodstream;
• Deficiency of coloring pigment and red cells per unit volume of blood;
• Significant increase in size of the spleen and liver.

Jaundice develops soon after the baby is born, sometimes within 24 hours. It progresses over time.

The baby's skin and mucous membranes become yellow, even orange. The severity of the disease depends on how early it appears. The more bilirubin accumulates in the blood, the more lethargic and drowsiness the child develops. There is suppression of reflexes and a decrease in muscle tone.

On days 3–4, the concentration of toxic bilirubin becomes critical - more than 300 micromol per liter.

Jaundice takes on a nuclear form when the subcortical nuclei of the brain are affected. This can be understood by stiff neck and opisthotonus, the “setting sun” symptom, a high-pitched cerebral scream. By the end of the week, the skin becomes greenish, the stool becomes colorless, and the level of direct bilirubin increases.

Diagnostics

It is necessary to carry out prenatal diagnosis of conflict immune system mother and fetus. At risk are women with miscarriages, stillbirths, or children who died on the first day from jaundice if the mothers received a blood transfusion without taking into account the Rh factor.

• It is necessary to determine the Rh and ABO group of the child’s parents. A mother with negative and a fetus with positive Rh are at risk. The father's genotype is checked to predict the Rh factor of future children. Women with blood group I are also in a dangerous situation.
• If the woman is Rh negative, the dynamics of the titer of anti-Rh antibodies are checked at least three times during pregnancy.
• Amniotic fluid is collected at 34 weeks if there is a risk.
• An ultrasound examination is required to check for thickening of the placenta and polyhydramnios.

Postpartum diagnostics are also carried out based on clinically manifested symptoms during and immediately after childbirth, as well as laboratory indicators of the disease. Consultation scheduled pediatric hematologist, who will supervise treatment if pathology is identified.

Treatment

In severe forms of the disease, treatment is as follows:

• A blood transfusion is performed with replacement (the “bad” blood is released and the donor blood is transfused);
• Hemosorption is carried out - blood is passed through or resins capable of absorbing toxic substances;
• A certain amount of blood is taken and plasma containing toxic components is removed from it.

Exchange transfusion helps remove indirect bilirubin and harmful antibodies from the baby's blood and increase the number of red blood cells.

• Be sure to read:

To carry out such a transfusion, blood with a negative Rh and the same ABO group as that of the baby is used. Now they are trying not to transfuse whole blood, so as not to reduce the risk of transmitting HIV or hepatitis, but to use a mass of Rh-negative red blood cells or plasma, depending on the ABO group.

If the disease has light form or carried out surgical treatment, do the following:

• Glucose and protein-based drugs are infused intravenously;
• Inducers of microsomal liver enzymes are prescribed;
• Vitamins C, E, group B, cocarboxylase, which improve liver functioning and normalize metabolic processes.

If syndromic thickening of bile is observed, choleretic drugs are prescribed internally. If anemia is severe, a red blood cell transfusion is given. At the same time, phototherapy is prescribed, that is, the child’s body is irradiated with a fluorescent lamp of white or blue light. Indirect bilirubin found in the skin is oxidized, forming water-soluble components that are excreted naturally.

Complications and consequences

If the disease is severe, complications can be the most disappointing, despite treatment:

• The fetus may die during pregnancy or in the first week after birth;
• The child may become disabled, including cerebral palsy;
• May completely lose hearing or go blind;
• Psychomotor impairment may occur;
• May develop due to stagnation of bile;
• Mental disorders are often observed.

The baby's red blood cells may have different properties from those of the mother. If the placenta allows such red blood cells to pass through, they turn into foreign antigens, and the response is the production of antibodies by the mother’s body. The penetration of antibodies into the fetus can cause:

• Hemolysis (decomposition of red blood cells);
• Extremely dangerous jaundice.

Prevention

Prevention of hemolytic disease is divided into specific and nonspecific:

• For nonspecific prophylaxis, transfusion is carried out taking into account the group and Rh factor and pregnancies are maintained;
• For specific prevention, anti-D immunoglobulin is administered on the first or second day immediately after childbirth (if there is a Rhesus conflict between mother and child) or abortion.

If the concentration of antibodies in the blood increases during pregnancy, the following is used:

• Hemosorption;
• 3-4 times intrauterine replacement blood transfusion at the 27th week using washed O(I) group O(I) Rh-negative red blood cells and subsequent delivery from the 29th week of pregnancy.

Hemolytic disease of the fetus and newborn - dangerous disease, which can and should be prevented in time, even in the early stages of pregnancy, be observed by specialists.