Angina

Inheritance of rh factor hemolytic disease of the fetus. Hemolytic disease

Hemolytic disease of the newborn (HDN) is a very common disease. This pathology is registered in approximately 0.6% of children born. Despite the development of various treatment methods, the mortality rate from this disease reaches 2.5%. Unfortunately, a large number of scientifically unsubstantiated “myths” are widespread about this pathology. For a thorough understanding of the processes occurring during hemolytic disease, knowledge of normal and pathological physiology, as well as, of course, obstetrics is necessary.

What is hemolytic disease of the newborn?

TTH is a consequence of a conflict between the immune systems of mother and child. The disease develops due to the incompatibility of the blood of a pregnant woman with antigens on the surface of the fetal red blood cells (primarily this). Simply put, they contain proteins that are recognized by the mother’s body as foreign. That is why the processes of activation of her immune system begin in the body of a pregnant woman. What's going on? So, in response to the ingress of an unfamiliar protein, the biosynthesis of specific molecules occurs that can contact the antigen and “neutralize” it. These molecules are called antibodies, and the combination of antibody and antigen is called immune complexes.

However, in order to get a little closer to a true understanding of the definition of HDN, it is necessary to understand the human blood system. It has long been known that blood contains different types of cells. The largest number of cellular composition is represented by erythrocytes. At the current level of development of medicine, at least 100 different systems of antigenic proteins present on the erythrocyte membrane are known. The most well studied are the following: rhesus, Kell, Duffy. But, unfortunately, there is a very common misconception that hemolytic disease of the fetus develops only according to group or Rh antigens.

The lack of accumulated knowledge about erythrocyte membrane proteins does not mean that incompatibility with this particular antigen in a pregnant woman is excluded. This is the debunking of the first and, perhaps, the most basic myth about the causes of this disease.

Factors causing immune conflict:

Video: about the concepts of blood group, Rh factor and Rh conflict

Probability of conflict if the mother is Rh-negative and the father is Rh-positive

Very often, a woman who is Rh negative worries about her future offspring, even without being pregnant. She is afraid of the possibility of developing a Rhesus conflict. Some are even afraid to marry an Rh-positive man.

But is this justified? And what is the likelihood of developing an immunological conflict in such a couple?

Fortunately, the Rh trait is encoded by so-called allelic genes. What does it mean? The fact is that the information located in the same areas of paired chromosomes can be different:

The allele of one gene contains a dominant trait, which is the leading one and is manifested in the organism (in our case, the Rh factor is positive, let’s denote it with a capital letter R);
A recessive trait that does not manifest itself and is suppressed by a dominant trait (in this case, the absence of the Rh antigen, let’s denote it with a small letter r).

What does this information tell us?

The bottom line is that a person who is Rh positive can contain either two dominant traits (RR) or both dominant and recessive (Rr) on their chromosomes.

Moreover, a mother who is Rh negative contains only two recessive traits (rr). As you know, during inheritance, each parent can give only one trait to their child.

Table 1. The probability of inheritance of a Rh-positive trait in a fetus if the father is a carrier of a dominant and recessive trait (Rr)

Table 2. Probability of inheriting a Rh-positive trait in a fetus if the father is a carrier of only dominant traits (RR)

	Mother (r) (r)	Father (R) (R)
Child	(R)+(r) Rh positive	(R)+(r) Rh positive
Probability	100%	100%

Thus, in 50% of cases, there may not be an immune conflict at all if the father is a carrier of the recessive trait of the Rh factor.

So, we can draw a simple and obvious conclusion: the judgment that an Rh-negative mother and an Rh-positive father must necessarily have immunological incompatibility is fundamentally wrong. This is the “exposure” of the second myth about the causes of the development of hemolytic disease of the fetus.

In addition, even if the child still has a positive Rh factor, this does not mean that the development of tension-type headache is inevitable. Don't forget about the protective properties. During a physiological pregnancy, the placenta practically does not allow antibodies to pass from mother to child. Proof is the fact that hemolytic disease occurs only in the fetus of every 20th Rh-negative woman.

Forecast for women with a combination of negative Rh and first blood group

Having learned about the identity of their blood, women with a similar combination of group and Rhesus fall into panic. But how justified are these fears?

At first glance, it may seem that the combination of “two evils” will create a high risk of developing TTH. However, ordinary logic does not work here. It's the other way around: the combination of these factors, oddly enough, improves the prognosis. And there is an explanation for this. In the blood of a woman with the first blood group there are already antibodies that recognize a foreign protein on red blood cells of a different group. This is how nature intended, these antibodies are called agglutinins alpha and beta, all representatives of the first group have them. And when a small amount of fetal red blood cells enters the mother’s bloodstream, they are destroyed by existing agglutinins. Thus, antibodies to the Rh factor system simply do not have time to form, because agglutinins are ahead of them.

Women with the first group and negative Rh have a small titer of antibodies against the Rh system, and therefore hemolytic disease develops much less frequently.

Which women are at risk?

Let us not repeat that negative Rh or first blood group is already a certain risk. However, It is important to know about the existence of other predisposing factors:

1. Blood transfusion in an Rh-negative woman during her life

This is especially true for those who have had various allergic reactions after a transfusion. Often in the literature one can find the judgment that those women who received a blood type transfusion without taking into account the Rh factor are at risk. But is this possible in our time? This possibility is practically excluded, since Rhesus status is checked at several stages:

During blood collection from a donor;
At the transfusion station;
The hospital laboratory where blood transfusions are performed;
A transfusiologist who conducts a three-time compatibility test between the blood of the donor and the recipient (the person receiving the transfusion).

The question arises: Where then is it possible for a woman to become sensitized (presence of hypersensitivity and antibodies) to Rh-positive erythrocytes?

The answer was given quite recently, when scientists found out that there is a group of so-called “dangerous donors” whose blood contains red blood cells with a weakly expressed Rh-positive antigen. It is for this reason that their group is defined by laboratories as Rh negative. However, when such blood is transfused, the recipient’s body may begin to produce specific antibodies in a small volume, but even their quantity is sufficient for the immune system to “remember” this antigen. Therefore, in women with a similar situation, even in the case of their first pregnancy, an immune conflict may arise between her body and the child.

2. Repeated pregnancy

It is believed that in During the first pregnancy, the risk of developing an immune conflict is minimal. And the second and subsequent pregnancies already occur with the formation of antibodies and immunological incompatibility. And this is true. But many people forget that the first pregnancy should be considered the fact of the development of the fertilized egg in the mother’s body to any term.

Therefore, women who have had:

Spontaneous abortions;
Frozen pregnancy;
Medical and surgical termination of pregnancy, vacuum aspiration of the fetal egg;
Ectopic pregnancy (tubal, ovarian, abdominal).

Moreover, primigravidas with the following pathologies are also at increased risk:

Chorionic detachment, placenta during this pregnancy;
Formation of a retroplacental hematoma;
Bleeding with low placenta previa;
Women who have had invasive diagnostic methods used (puncture of the amniotic sac with collection of amniotic fluid, taking blood from the fetal umbilical cord, biopsy of the chorionic villus, examination of the placenta after 16 weeks of pregnancy).

Obviously, the first pregnancy does not always mean the absence of complications and the development of an immune conflict. This fact dispels the myth that only the second and subsequent pregnancies are potentially dangerous.

What is the difference in hemolytic disease of the fetus and newborn?

There are no fundamental differences in these concepts. Simply hemolytic disease in the fetus occurs in the prenatal period. HDN means the occurrence of a pathological process after the birth of a child. Thus, the difference lies only in the conditions under which the baby is staying: in utero or after birth.

But there is one more difference in the mechanism of this pathology: during pregnancy, maternal antibodies continue to enter the fetus’s body, which lead to a deterioration in the condition of the fetus, while after childbirth this process stops. That's why women who have given birth to a baby with hemolytic disease are strictly prohibited from feeding their baby breast milk. This is necessary in order to prevent the entry of antibodies into the baby’s body and not to aggravate the course of the disease.

How does the disease progress?

There is a classification that well reflects the main forms of hemolytic disease:

1. Anemic– the main symptom is a decrease in fetus, which is associated with the destruction of red blood cells () in the baby’s body. Such a child has all the signs:

2. Edema form. The predominant symptom is the presence of edema. A distinctive feature is the deposition of excess fluid in all tissues:

In subcutaneous tissue;
In the chest and abdominal cavity;
In the pericardial sac;
In the placenta (during the prenatal period)
Hemorrhagic skin rashes are also possible;
Sometimes there is a dysfunction of blood clotting;
The child is pale, lethargic, weak.

3. Jaundice form characterized by, which is formed as a result of the destruction of red blood cells. This disease causes toxic damage to all organs and tissues:

The most severe option is the deposition of bilirubin in the liver and brain of the fetus. This condition is called “kernicterus”;
A yellowish coloration of the skin and sclera of the eyes is characteristic, which is a consequence of hemolytic jaundice;
It is the most common form (in 90% of cases);
Diabetes mellitus may develop if the pancreas is damaged.

4. Combined (the most severe) - is a combination of all previous symptoms. It is for this reason that this type of hemolytic disease has the highest mortality rate.

How to determine the severity of the disease?

In order to correctly assess the child’s condition, and most importantly, prescribe effective treatment, it is necessary to use reliable criteria when assessing the degree of severity.

Diagnostic methods

Already during pregnancy, it is possible to determine not only the presence of this disease, but even the severity.

The most common methods are:

1. Determination of the titer of Rh or group antibodies. It is believed that a titer of 1:2 or 1:4 is not dangerous. But this approach is not justified in all situations. Here lies another myth that “the higher the titer, the worse the prognosis.”

The antibody titer does not always reflect the real severity of the disease. In other words, this indicator is very relative. Therefore, it is necessary to assess the condition of the fetus using several research methods.

2. Ultrasound diagnostics is a very informative method. The most characteristic signs:

Placenta enlargement;
The presence of fluid in the tissues: tissue, chest, abdominal cavity, swelling of the soft tissues of the fetal head;
Increased blood flow speed in the uterine arteries and in the vessels of the brain;
Presence of suspension in amniotic fluid;
Premature aging of the placenta.

3. Increased density of amniotic fluid.

4. Upon registration - signs and disturbances of heart rhythm.

5. In rare cases, cord blood testing is performed(determine the level of hemoglobin and bilirubin). This method is dangerous due to premature termination of pregnancy and fetal death.

6. After the birth of a child, there are simpler diagnostic methods:

Taking blood to determine: hemoglobin, bilirubin, blood group, Rh factor.
Examination of the child (in severe cases, jaundice and swelling are evident).
Determination of antibodies in the child's blood.

Treatment of tension-type headache

Treatment for this disease can begin now. during pregnancy, to prevent deterioration in the condition of the fetus:

Introduction of enterosorbents into the mother’s body, for example “Polysorb”. This drug helps reduce the antibody titer.
Drip administration of solutions of glucose and vitamin E. These substances strengthen the cell membranes of red blood cells.
Injections of hemostatic drugs: “Ditsinon” (“Etamzilat”). They are needed to increase blood clotting ability.
In severe cases, intrauterine delivery may be required. However, this procedure is very dangerous and is fraught with adverse consequences: fetal death, premature birth, etc.

Methods of treating a child after childbirth:

For severe disease, the following treatment methods are used:

Blood transfusion. It is important to remember that only “fresh” blood is used for blood transfusion, the date of collection of which does not exceed three days. This procedure is dangerous, but it can save the baby's life.
Blood purification using hemodialysis and plasmapheresis machines. These methods help remove toxic substances from the blood (bilirubin, antibodies, products of red blood cell destruction).

Prevention of the development of immune conflict during pregnancy

Women at risk for developing immunological incompatibility You must adhere to the following rules, there are only two of them:

Try not to have an abortion; to do this, you need to consult a gynecologist to prescribe reliable methods of contraception.
Even if the first pregnancy went well, without complications, then after birth, within 72 hours it is necessary to administer anti-Rhesus immunoglobulin (“KamROU”, “HyperROU”, etc.). The completion of all subsequent pregnancies should be accompanied by the administration of this serum.

Hemolytic disease of the newborn is a serious and very dangerous disease. However, you should not unconditionally believe all the “myths” about this pathology, even though some of them are already firmly rooted among most people. A competent approach and strict scientific validity are the key to a successful pregnancy. In addition, it is necessary to pay due attention to prevention issues in order to avoid potential problems as much as possible.

Description:

Hemolytic disease of the fetus and newborn is an immune conflict between the body of the mother and the fetus. The mother's body synthesizes antibodies in response to fetal erythrocyte antigens that are foreign to it. The most common type of immunological incompatibility between mother and fetus is Rh factor incompatibility - 97%; blood group incompatibility is much less common. The Rh factor in the fetus is detected at the 8th -9th week of intrauterine development, the number of Rh antigens gradually increases. They penetrate the mother's blood through the placenta and anti-Rhesus antibodies are formed against them if the mother is Rh-negative. Penetrating through the placenta into the fetus, maternal antibodies cause the breakdown of red blood cells. This is associated with the second name of this pathology - erythroblastosis. Develops, with hemolysis an increased amount of bilirubin is formed; As compensatory mechanisms in the fight against anemia, foci of hematopoiesis are formed in the liver and spleen of the fetus, which leads to an increase in these organs and disruption of their function.

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. 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 cause of hemoloitic disease is 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 ABO 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.

Symptoms of hemolytic disease of the fetus and newborn:

Hemolytic anemia is the mildest 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 HMB 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.
in combination with jaundice - occurs more often, is characterized as a more severe form of the disease. Characterized by hyper- or normochromic anemia, jaundice and hepatosplenomegaly. Amniotic fluid has an icteric coloration, as do vernix, umbilical cord, membranes and umbilical cord. The content of indirect bilirubin is 10-20 µmol/l above the upper limit of normal. The condition of the newborn is serious and worsening. If the hourly increase in bilirubin is 5-10 times, then “kernicterus” develops, 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, omphalitis, are often added. After 7 days of life, the pathogenic effect of antibodies entering the fetal blood ceases.

Hemolytic anemia in combination with jaundice and dropsy is 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. May be developing. 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.

Diagnostics:

All women who have given birth to children with hemolytic disease and all women who have been found to have Rh sensitization are subject to observation by an obstetrician and immunologist. The titer of Rh antibodies is determined in the blood of women once a month until the 32nd week of pregnancy; 2 times a month from 32 to 35 weeks and weekly from the 36th week.

In the antenatal diagnosis of hemolytic disease, ultrasound is important, in which signs such as an increase in the size of the liver and spleen, thickening of the placenta, and fetal hydrops can be detected. According to indications and doctor's prescription, amniotic fluid is examined, which is obtained by puncture of the amniotic sac (amniocentesis). The puncture is performed through the abdominal wall. The location of the placenta and fetus is first determined by ultrasound to avoid injury during puncture. In the amniotic fluid, the content of antibodies, the bilirubin level, and the blood group of the fetus are determined - which are essential for assessing its condition and prescribing appropriate therapy. According to indications, cordocentesis is also performed - taking blood from the fetal umbilical cord.

Treatment of hemolytic disease:

The following methods are most effective:

Content:

One of the common pathologies that occurs in pregnant women is hemolytic disease of the fetus. It develops on the basis of an immune conflict between the organisms of the mother and the unborn child. Immunological incompatibility is associated with a conflict over the Rh factor. Its manifestation is observed in 97% of cases. It is much less common to find incompatible blood groups. Under the influence of pathological mechanisms, the functions of the liver and spleen are disrupted.

What is hemolytic disease?

Hemolytic disease of the fetus is considered a pathological abnormality that occurs during intrauterine development. Its essence lies in the immunological conflict between the maternal body and the fetus. This situation arises due to the incompatibility of the blood composition of the mother and child, which contains different amounts of antigens.

As a result of such a conflict, red blood cells die in the fetal body. Maternal antibodies overcome the protective barrier of the placenta and help remove hemoglobin from red blood cells. During their breakdown, toxic elements are formed, which increase the amount of bilirubin and immature red blood cells. This occurs when the fetus has paternal antigens, but the mother does not have them. Such a disorder causes anemia, jaundice and edema, and sometimes the death of the unborn child.

The cause of hemolytic disease is the development of a conflict between different Rh factors. Sometimes there is incompatibility in blood groups and some types of antigens. Timely detection of pathology in combination with proper treatment increases the chances of a favorable prognosis.

Causes of hemolytic disease

The main cause of the pathology is an immunological conflict associated with blood incompatibility. In this case, the maternal Rh factor is negative, and the fetus is positive. Thus, a Rh conflict arises, especially when this is not the woman’s first pregnancy.

A serious reason is incompatibility of blood groups. The mother has group 1, and the child has any other group. When there is a conflict between antigens A and B, which enter the maternal blood through the placenta, protective antibodies are produced. Next, a conflict arises between antigens and antibodies. Such incompatibility often develops already during the first pregnancy, but occurs in a milder form.

In rare cases, conflicts can occur between different types of antigens. Basically, these are M, N, S and P antigens, the Duffy, Kell systems and other factors that can cause incompatibility.

Symptoms and signs

The early stage of the disease occurs without any specific features and is practically undetectable. Pregnancy proceeds normally, without deviations. With further intrauterine development of the fetus, symptoms are observed that manifest themselves on an individual basis.

The main manifestations of hemolytic disease:

The most severe manifestation is associated with intrauterine fetal death, occurring between the 20th and 30th weeks of development. In the absence of a timely ultrasound or blood tests, the deceased child may remain in the womb for 10 - 14 days. There is no bleeding, and the woman feels well and does not suspect anything. Failure to take immediate action can lead to blood poisoning and other unpleasant consequences.
The occurrence of edema in the fetus, manifested in the growth of its weight. Fiber gradually accumulates in the body, internal organs enlarge, including the heart, liver, kidneys and spleen. There is an increase in the size of the placenta. Severe anemia often leads to fetal death. This can happen in the womb or during childbirth.
With the icteric type of fetal disease, pregnancy proceeds as usual and ends in natural birth. Further measures are carried out in relation to an already born child a couple of hours after his birth. Bilirubin appears in the baby’s blood, causing irreversible processes.
The mildest manifestations are observed in anemic hemolytic disease. A newly born fetus looks pale, flaccid, cyanotic, with a vascular network located on the body.

Diagnostics

Diagnostic measures are carried out when the fetus's hemoglobin level decreases and the amount of bilirubin contained in the body increases. Red blood cells containing antibodies are detected using a direct Coombs test. To test maternal serum with incomplete antibodies, an indirect Coombs test is used. The identified Rh conflicts give reason to assume the presence of incompatibility.

Further studies for Rh incompatibility are carried out through antenatal diagnosis. For this purpose, the behavior of antibodies in the maternal serum in relation to the Rh antigen D is studied. An ultrasound examination of the fetus and placenta is first performed, after which direct antenatal diagnosis is carried out by transabdominal amniocentesis.

At the same time, dynamic studies of the amount of bilirubin are performed, especially if its level increases.

Treatment of hemolytic disease of the fetus

For treatment to be effective, Rh conflict must be established during fetal development. The severity of the pathology is preliminarily assessed, and a prognosis is made, allowing treatment to be prescribed as early as possible. All treatment activities are carried out in two main areas.

Treatment with non-invasive methods includes plasmapheresis, immunoglobulin administered intravenously to the pregnant woman. Contraindications to plasmapheresis are a weak immune system, the presence of severe cardiovascular diseases, anemia, allergic reactions to the administration of anticoagulants, protein and colloid drugs.

In another direction, hemolytic disease of the fetus is treated with invasive methods. This includes cordocentesis and intrauterine transfusion of the entire mass of red blood cells. These measures are carried out with low hemoglobin and hematocrit during a certain period of pregnancy.

Hemolytic disease of the fetus and newborn (HDN)

ICD 10: P55

Year of approval (revision frequency): 2016 (reviewed every 3 years)

ID: KR323

Professional associations:

Russian Association of Perinatal Medicine Specialists

Approved

Russian Association of Perinatal Medicine Specialists 2016

Agreed

Scientific Council of the Ministry of Health of the Russian Federation__ __________201_

newborn

phototherapy

replacement blood transfusion surgery

kernicterus

hydrops fetalis

Rhesus – isoimmunization of the fetus and newborn

ABO - isoimmunization of the fetus and newborn

List of abbreviations

AG? antigen

HELL? blood pressure

ALT? alanine aminotransferase

AST? aspartate aminotransferase

AT? antibody

BE? bilirubin encephalopathy

HDN? hemolytic disease of the newborn

GGT? gamma-glutamyl transpeptidase

ICE? disseminated intravascular coagulation

KOS? acid-base state

ICD? international classification of diseases -10

ABOUT? total bilirubin

OZPK? replacement blood transfusion surgery

NICU? neonatal intensive care unit

OCC? circulating blood volume

PICU - neonatal resuscitation and intensive care unit

FFP - fresh frozen plasma

FT? phototherapy

BH? respiration rate

Heart rate? heart rate

alkaline phosphate? alkaline phosphatase

Hb? hemoglobin

IgG? immunoglobulin G

IgM? immunoglobulin M

Terms and definitions

– isoimmune hemolytic anemia, which occurs in cases of incompatibility between the blood of mother and fetus for erythrocyte antigens, while the antigens are localized on the erythrocytes of the fetus, and antibodies to them are produced in the mother’s body.

1. Brief information

1.1 Definition

Hemolytic disease of the fetus and newborn (HDN)– isoimmune hemolytic anemia, which occurs in cases of incompatibility of the blood of mother and fetus with respect to erythrocyte antigens (AGs), while the AGs are localized on the erythrocytes of the fetus, and antibodies (AB) to them are produced in the mother’s body.

1.2 Etiology and pathogenesis

The occurrence of an immunological conflict is possible if antigens are present on the fetal red blood cells that are absent on the cell membranes of the mother. Thus, the immunological prerequisite for the development of HDN is the presence of an Rh-positive fetus in an Rh-negative pregnant woman. In case of an immunological conflict due to group incompatibility, in most cases the mother’s blood type is determined to be O (I), and that of the fetus is A (II) or (less often) B (III). More rarely, HDN develops due to a mismatch between the fetus and the pregnant woman in other group (Duff, Kell, Kidd, Lewis, MNSs, etc.) blood systems.

Previous isosensitization due to abortion, miscarriage, ectopic pregnancy, childbirth, during which the mother’s immune system produces antibodies to erythrocyte antigens, predisposes the entry of fetal erythrocytes into the mother’s bloodstream and the occurrence of an immunological conflict in cases of antigenic incompatibility with blood factors. If the antibodies belong to class G immunoglobulins (subclasses IgG1, IgG3, IgG4)? they freely penetrate the placenta. With an increase in their concentration in the blood, the likelihood of developing hemolytic disease of the fetus and newborn increases. Antibodies of the IgG2 subclass have a limited ability of transplacental transport; antibodies of the IgM class, which include β- and β-agglutinins, do not penetrate the placenta.

The implementation of HDN according to the Rh factor, as a rule, usually occurs with repeated pregnancies, and the development of HDN as a result of a conflict according to group blood factors is possible already during the first pregnancy. If there are immunological prerequisites for the implementation of both options, HDN often develops according to the ABO system. In this case, the occurrence of hemolysis due to the entry of group II maternal anti-A antibodies into the child’s blood is more common than when group III anti-B antibodies enter the child’s blood. However, in the latter case, the penetration of anti-B antibodies leads to more severe hemolysis, often requiring replacement blood transfusion. The severity of the child's condition and the risk of developing kernicterus with HDN according to the ABO system are less pronounced compared to HDN according to the Rh factor. This is explained by the fact that group antigens A and B are expressed by many cells of the body, and not just red blood cells, which leads to the binding of a significant amount of antibodies in non-hematopoietic tissues and prevents their hemolytic effects.

1.3 Epidemiology

HDN in Russia is diagnosed in approximately 0.6% of all newborns.

1.4 Codes according to ICD 10

Hemolytic disease of the fetus and newborn(P55):

P55.0 - Rhesus - isoimmunization of the fetus and newborn

P55.1 - ABO - isoimmunization of the fetus and newborn

P55.8 - Other forms of hemolytic disease of the fetus and newborn

P55.9 - Hemolytic disease of fetus and newborn, unspecified

1.5 Classification

1.5.1 Regarding the conflict between mother and fetus according to the ABO system and other erythrocyte blood factors:

incompatibility according to the ABO system;
incompatibility of maternal and fetal red blood cells according to the Rh factor;
incompatibility for rare blood factors.

1.5.2 Based on clinical manifestations, the following forms of the disease are distinguished:

edematous (hemolytic anemia with dropsy);

icteric (hemolytic anemia with jaundice);

anemic (hemolytic anemia without jaundice and dropsy).

1.5.3 According to the severity of jaundice in the icteric form:

medium severity;

severe degree.

1.5.4 According to the presence of complications:

bilirubin encephalopathy: acute damage to the central nervous system;

kernicterus: irreversible chronic damage to the central nervous system;

bile thickening syndrome;

hemorrhagic syndrome.

2. Diagnostics

2.1 Complaints and anamnesis

When collecting anamnesis, it is recommended to pay attention to:

Rhesus - mother's blood type and blood type;

infections during pregnancy and childbirth;

hereditary diseases (G6PD deficiency, hypothyroidism, other rare diseases);

presence of jaundice in parents;

the presence of jaundice in a previous child;

weight and gestational age of the baby at birth;

feeding the child (insufficient feeding and/or vomiting).

2.2 Physical examination

Edematous form of HDN

General edematous syndrome (anasarca, ascites, hydropericardium), severe pallor of the skin and mucous membranes, hepatomegaly and splenomegaly, jaundice is absent or mild. Hemorrhagic syndrome and development of disseminated intravascular coagulation syndrome are possible.

Jaundice form of HDN

At birth, the amniotic fluid, umbilical cord membranes, and vernix may be jaundiced. Characteristic is the early development of jaundice, pallor of the skin and visible mucous membranes, enlargement of the liver and spleen.

Anemic form of HDN

Against the background of pallor of the skin, lethargy, poor sucking, tachycardia, an increase in the size of the liver and spleen are noted, muffled heart sounds and systolic murmur are possible.

Complications of tension-type headache

Kernicterus - bilirubin intoxication - lethargy, loss of appetite, regurgitation, pathological yawning, muscle hypotonia, disappearance of the 2nd phase of the Moro reflex, then a clinic of encephalopathy appears - opisthotonus, "brain" cry, bulging of the large fontanel, convulsions, pathological oculomotor symptoms - a symptom of "setting" sun", nystagmus. Bile thickening syndrome - jaundice acquires a greenish tint, the liver is enlarged, and the urine is rich in color.

2.3 Laboratory diagnostics

It is recommended to establish the Rh factor already in the first hours of a child’s life based on anamnesis (increase in the titer of anti-D antibodies in Rh(–)

All women with a negative Rh factor during pregnancy are recommended to determine the level of immune antibodies in the blood over time.

Comments:TTH according to the AB0 system, as a rule, does not have specific signs in the first hours after birth.

If the mother’s blood is characterized by a negative Rh factor or belongs to O (I) group, the newborn is recommended to conduct a study of the concentration of total bilirubin in the umbilical cord blood and determine the blood type and Rh factor

Group and Rh affiliation of the blood of mother and child.
General blood test.
Biochemical blood test (total bilirubin and fractions, albumin, glucose level; other parameters (bilirubin fractions, acid-base state (ABS), electrolytes, etc.) - according to indications);
Serological tests: Coombs test.

Comments:The direct Coombs test becomes positive in the presence of fixed antibodies on the surface of red blood cells, which is usually observed in HDN due to the Rh factor. Due to the small amount of antibodies fixed on erythrocytes, with ABO HDN, a weakly positive direct Coombs test is more often observed in the first day of life, which can already become negative 2-3 days after birth.

The indirect Coombs test is designed to detect incomplete antibodies present in the test serum. This is a more sensitive test for detecting maternal isoantibodies than the direct Coombs test. The indirect Coombs test can be used in individual cases when the cause of hemolysis is unclear.

It should be remembered that the severity of the Coombs reaction does not correlate with the severity of jaundice! (Level of Evidence D)

2.4 Instrumental diagnostics

An abdominal ultrasound is recommended;

Neurosonography is recommended.

2.5 Other diagnostics

It is recommended to conduct laboratory and blood tests:

blood for ELISA (for the presence of infection);

blood for PCR (for the presence of infection);

coagulogram;

bacteriological blood test.

3. Treatment

3.1 Conservative treatment

Comments:Features of PT for HDN:

It is possible to use both standard lamps and fiber-optic and LED FT; it is advisable to combine several FT methods;

The light source is located at a distance of 50 cm above the child. To enhance the effect of phototherapy, the lamp can be brought closer to a distance of 10-20 cm from the child with constant supervision of medical personnel and monitoring of body temperature;

Phototherapy for tension-type headaches (especially in children at risk of acute onset) should be carried out continuously;

The surface of the child's body against the background of PT should be as open as possible. The diaper can be left in place;

Eyes and genitals should be protected with light-proof material;

The daily volume of fluid that the child receives enterally or parenterally must be increased by 10-20% compared to the child’s physiological need;

12 hours after the end of phototherapy, it is necessary to perform a control test of bilirubin;

Phototherapy is carried out before, during (using a fiberoptic system) and after an exchange blood transfusion.

Intravenous administration of normal human immunoglobulin is recommended. High doses of standard immunoglobulins block Fc receptors of cells of the reticuloendothelial system and thereby reduce hemolysis and, consequently, the level of bilirubin, which in turn reduces the number of OPCs.

Comments:Human immunoglobulin preparations are administered to newborns with HDN according to the following scheme:

in the first hours of a newborn’s life, intravenously slowly (if possible, within 2 hours), but with mandatory compliance with the instructions for the drug;

dose? 0.5-1.0 g/kg (average 0.8 g/kg)*

*If a dose of immunoglobulin is prescribed that exceeds that specified in the instructions for the drug, it is necessary to substantiate this action in as much detail as possible in the medical history and obtain a collegial permission to administer “Off-label” therapy to the child. The use of “off-label” therapy also requires mandatory registration of voluntary informed consent from the patient’s legal representative, which explains in detail the specifics of the use of such therapy, possible risks and side effects, and also explains the right to refuse “off-label” therapy. label";

repeated administration of immunoglobulin, if necessary, is carried out 12 hours from the previous one;

administration of immunoglobulin for HDN is possible during the first 3 days of life.

Comments:The exception is when breast milk is not enough to increase the daily volume by 10-20%. If the child’s condition does not allow increasing the volume of fluid enterally, only then is infusion therapy performed.

Administration of human albumin. There is no evidence that human albumin infusion improves long-term outcomes in children with severe hyperbilirubinemia and its routine use is not recommended.

Phenobarbital** – the effect on tension-type headache has not been proven, use is not permissible.

Other medications (drugs of the hepatoprotector group) - use for tension-type headache has not been proven and is not permissible.

3.2 Surgical treatment

Comments:Indications for OZPK:

in the event of the appearance of clinical symptoms of acute bilirubin encephalopathy (muscle hypertonicity, opisthotonus, fever, “brain scream”), a replacement blood transfusion is carried out regardless of the bilirubin level;

in case of HDN caused by an isolated Rhesus conflict, Rh-negative same-group EM and FFP, if possible, AB (IV) blood group with the child’s blood are used in the ratio of EM to FFP - 2:1;

in case of tension-type headache caused by an isolated group conflict, the first (I) group EO is used, which matches the Rhesus status of the child’s red blood cells and the same group or AB (IV) group FFP in a ratio of 2:1;

If the mother's blood and the child's blood are incompatible due to rare factors, it is necessary to use blood from individually selected donors.

For HDN, only freshly prepared EO is used (shelf life no more than 72 hours);

OPC is performed under aseptic conditions in the intensive care unit or operating room;

During the operation, monitoring of heart rate, breathing, blood pressure, hemoglobin oxygen saturation, and body temperature should be provided. Before the operation begins, the patient is given a nasogastric tube;

Transfusion is performed through the umbilical vein using a polyvinyl catheter (No. 6, 8, 10). The depth of catheter insertion depends on the patient’s body weight (no more than 7 cm).

Calculation of volume for OZPK

V total = m?BCC?2, where V is volume, m is body weight in kg,

BCC – for premature babies – 100-110 ml/kg, for full-term babies – 80-90 ml/kg.

Example: a child weighing 3 kg.

Total volume (V total) = 3?85?2 = 510 ml

Absolute volume of red blood cells (V abs.) required to obtain Ht 50% V total: 2 = 510: 2 = 255 ml

Actual volume of EV

(V era.mass) = Vabs: 0.7 (approximate Ht of red blood cells) = 255: 0.7 = 364 ml

Actual volume of FFP = V total. - V era. Masses = 510 – 364 = 146 ml

First, 10 ml of blood is released through the catheter, which is used to determine the concentration of bilirubin. Then the same volume of donor blood is injected at a rate of 3-4 ml/min.

The introduction and removal of blood alternate with a volume of 20 ml in full-term infants and 10 ml in premature infants.

The volume of one exfusion-infusion should not exceed 5-10% of the bcc. The total duration of the operation is about 2 hours.

After the operation, it is recommended to perform an OAM and two hours after the end of the transfusion, it is recommended to determine the concentration of glucose in the blood.

The effectiveness of the performed OPC is evidenced by a more than twofold decrease in bilirubin concentration at the end of the operation.

4. Rehabilitation

Rehabilitation measures are recommended:

neonatal care;

exclusive breastfeeding;

medical exemption from preventive vaccinations for 1 month.

5. Prevention and clinical observation

5.1 Prevention

Prevention of Rh immunization after childbirth is recommended for Rh-negative mothers who do not have anti-Rh antibodies and who gave birth to a Rh-positive child. Performed in the first 72 hours after birth by administering 300 mcg of anti-D(Rh) immunoglobulin.

Recommended:

observation by a local pediatrician or general practitioner;
every month control of UAC;
at 6 months for children after OPC - blood testing for HIV;
The issue of preventive vaccinations is decided after 6 months of life.

6. Additional information affecting the course and outcome of the disease

Additional factors that increase the risk of developing bilirubin encephalopathy:

Factors that increase the permeability of the BBB for bilirubin: blood hyperosmolarity, acidosis, cerebral hemorrhages, neuroinfections, arterial hypotension.
Factors that increase the sensitivity of brain neurons to the toxic effects of unconjugated bilirubin: prematurity, severe asphyxia, fasting, hypoglycemia, anemia.
Factors that reduce the ability of blood albumin to firmly bind unconjugated bilirubin: prematurity, hypoalbuminemia, infection, acidosis, hypoxia, increased levels of non-esterified fatty acids in the blood, the use of sulfonamides, furosemide, phenytoin, diazepam, indomethacin, salicylates, semisynthetic penicillins, cephalosporins.

Criteria for assessing the quality of medical care

Quality criteria	Level of evidence
A study was performed on the level of total bilirubin and the level of total hemoglobin in the umbilical cord blood of a newborn at birth (with a negative Rh factor and/or blood group 0(I) in the mother)
Determination of the main blood groups (A, B, 0) and determination of Rh in the newborn in umbilical cord blood at birth
A direct antiglobulin test (direct Coombs test) and/or an indirect antiglobulin test (Coombs test) was performed
A repeat study of the level of total bilirubin was performed and the hourly increase in total bilirubin was determined no later than 6 hours and 12 hours from the moment of birth
A general (clinical) blood test was performed to determine the number of reticulocytes: 7%
Skin phototherapy and/or exchange transfusion was performed after assessing the level of total bilirubin depending on birth weight (if indicated)	1	A
A partial exchange transfusion operation was performed no later than 3 hours from the moment of birth (for the edematous form of hemolytic disease)

References

Neonatology. National leadership. Brief edition / ed. acad. RAMS N.N. Volodina. ? M.: GEOTAR-Media, 2013. ? 896 pp.
New technologies in the diagnosis, treatment and prevention of hemolytic disease of the fetus and newborn, Konoplyannikov A.G. Abstract for the degree of Doctor of Medical Sciences, Moscow 2009
Edematous form of hemolytic disease of newborns (diagnosis, treatment, long-term results), Chistozvonova E.A. Abstract for the academic degree of Candidate of Medical Sciences, Moscow 2004
Order of the Ministry of Health of Russia dated November 1, 2012 N 572n “On approval of the Procedure for providing medical care in the field of obstetrics and gynecology (except for the use of assisted reproductive technologies).”
Order of the Ministry of Health of Russia dated November 15, 2012 N 921n “On approval of the Procedure for providing medical care in the field of neonatology.”
Order of the Ministry of Health of Russia dated April 2, 2013 N 183n “On approval of the rules for the clinical use of donor blood and (or) its components.”
Shabalov N.P. Neonatology / N.P.Shabalov. ? 5th ed., rev. and additional, in 2 volumes. ? M.: MEDpress-inform, 2009. ? 1504 pp.
ABM Clinical protocol 22: Guidelines for management of jaundice in the breastfeeding infant equal to or greater than 35 weeks gestation // Breastfeeding medicine. ? 2010. ? Vol. 5. ? N 2. ? P. 87-93.
Alcock G.S., Liley H. Immunoglobulin infusion for isoimmune haemolytic jaundice in neonates (Cochrane Review). In: The Cochrane Library, Issue 2, 2004. Chichester, UK: John Wiley & Sons, Ltd.
Altunyurt S., Okyay E., Saatli B., Canbahishov T., Demir N., Ozkan H. Neonatal outcome of fetuses receiving intrauterine transfusion for severe hydrops complicated by Rhesus hemolytic disease // Int. J. Gynaecol. Obstet. ? 2012. ? Vol. 117. ? N 2. ? P. 153-156.
Barrington K.J., Sankaran K. Canadian Pediatric Society Fetus and Newborn Committee Abridged version // Paediatr Child Health. ? 2007. ? Vol. 12. ? P. 1-12.
Buonocore G., Bracci R., Weindling M. Neonatology: A Practical Approach to Neonatal Management, 2012
Christensen RD, Henry E. Hereditary spherocytosis in neonates with hyperbilirubinemia // Pediatrics. ? 2010. ? Vol. 125. ? N 1. ? P. 120-125.
Gleason C.A., Devaskar S.U. Avery’s diseases of the newborn // 9th Ed. Elsevier Saunders. ? 2011. ? 1520 p.
Gomella T.L. Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs // 7th edition; Medical Publishing Division. ? 2013. ? 1113 p.
Hudon L., Moise K. J. Jr., Hegemier S. E., et al. Long-term neurodevelopmental outcome after intrauterine transfusion for the treatment of fetal hemolytic disease // Am J Obstet Gynecol. ? 1998. ? Vol. 179. ? N 4. ? R. 858-863.
Kaplan M., Na'amad M., Kenan A., et al. Failure to predict hemolysis and hyperbilirubinemia by IgG subclass in blood group A or B infants born to group O mothers // Pediatrics. ? 2009. ? Vol. 123. ? N 1. ? e132-137.
Maisels M.J., Watchoko J.F. Neonatology: A Practical Approach to Neonatal Management/ Treatmen of Hyperbilirubinemia- 2012- P 629
Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation // Pediatrics. ? 2004. ? Vol. 114. ? P. 297-316.
Mary Beth Ross, Pedro de Alarcon. Hemolytic Disease of Fetus and Newborn. NeoReviews Vol.14 No.2 February 2013
Matthews D.C., Glader B. Erythrocyte disorders in infancy // In: Avery’s diseases of the newborn. Ninth edition. Elsevier-Saunders. ? 2012. ? P. 1087-1092.
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Moise K.J. Jr. Management of Rhesus alloimmunization in pregnancy // Obstet Gynecol. ? 2008. ? Vol. 112. ? P. 164-176.
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Wagle S., Deshpande P.G., Itani O., Windle M.L., Clark D.A., Wagner C.l. Rosenkrantz T. Hemolytic Disease of Newborn. Updated: Sep 26, 2014. http://emedicine.medscape.com/article/974349
Oxford handbook of Neonatology Ed. Fox G., Hoque N., Watts T // Oxford, New York, Oxford University Press, 2010. - 523.

Appendix A1. Composition of the working group

Antonov A.G. ?

Aronskind E.V. ?

Baibarina E.N. ?

Volodin N.N. ? Doctor of Medical Sciences, Academician of the Russian Academy of Sciences, President of the Russian Association of Perinatal Medicine Specialists, Federal Scientific Clinical Center for Pediatric Hematology, Oncology and Immunology named after Dmitry Rogachev of the Russian Ministry of Health.

Degtyarev D.N. ?

Degtyareva A.V. ?

Kovtun O.P. ?

Mukhametshin F.G. ?

Parshikova O.V. ?

Doctor - Neonatology;

Doctor-Anesthesiology-Reanimatology;

Doctor-Pediatrics.

Methods used to collect/select evidence:

search in electronic databases.

Description of methods used to collect/select evidence: the evidence base for the recommendations is publications included in the Cochrane Library, MEDLINE and EMBASE databases. The search depth was 25 years.

Methods used to assess the quality and strength of evidence:

expert consensus;

Table P1 – Levels of evidence according to international criteria

Table P2 – Levels of Recommendation Strength

Good Practice Points (GPPs):

Economic analysis:

no cost analysis was performed and pharmacoeconomics publications were not reviewed.

External expert assessment;

Internal expert assessment.

Appendix A3. Related documents

International Classification of Diseases, Injuries and Conditions Affecting Health, 10th Revision (ICD-10) (World Health Organization) 1994.

Nomenclature of medical services (Ministry of Health and Social Development of the Russian Federation) 2011.

Federal Law “On the fundamentals of protecting the health of citizens in the Russian Federation” dated November 21, 2011 No. 323 F3.

List of vital and essential drugs for 2016 (Order of the Government of the Russian Federation dated December 26, 2015 No. 2724-r.)

The procedure for providing medical care in the specialty “neonatology” (Order of the Ministry of Health of Russia dated November 15, 2012 N 921n).

Appendix B. Patient management algorithms

Tactics for managing children with tension-type headache over 24 hours of age:

depends on the absolute values of bilirubin (Table 1) or the dynamics of these indicators.

if jaundice appears during the first 24 hours of life - an urgent study of OB, further management tactics depend on the amount of hourly increase in bilirubin;

order the necessary blood products (plasma + Ermassa), stabilize the vital functions of the body.

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 marking system designates them with 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 (i.e., 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 a large number of immature red blood cells are present in the patient’s blood - the result of increased activity of the bone marrow, which is in a hurry to replace adult blood cells that are dying under the influence of any factors. 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 of hemolytic disease of newborns begins during pregnancy, so its 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 turns all tissues yellow, including the mucous membranes of the mouth 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 blood hemoglobin levels.

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.

Enlarged liver and spleen. This happens in the first two to three days after birth.
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.
Discoloration of stool. It occurs against the background of darkening of urine, gas and regurgitation after eating. All these signs are explained by cholestasis - retention of bile in the 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 faded.

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 newborns 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 are conditionally suitable for use. 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 measures are carried out if it is not available at the time of the start of the procedure, since, otherwise, preventive 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, preventing them from entering the “negative” circulatory system of the mother. If there is no mixing of different types of blood, antibodies to the child’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. Among them are 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 in them. If they exist, in the future you need to beware of prescribing any (medical and traditional) medicines to your child. 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.