Anemia in newborns: hemolytic, iron deficiency, physiological. Hemolytic disease of the newborn - physiological jaundice

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 the incompatibility of the blood of the fetus and its mother, when a 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 the female body enter the body of the child. Thus, the 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 crumbs and anemia.

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

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

When a newborn begins to develop hemolysis or the destruction of red blood cells, the level of bilirubin in his blood rises very quickly 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 child

1. Edematous form of HDN. This form is the most severe and it begins to develop even in utero. As a result of the destruction of red blood cells, a child develops a severe form of anemia, metabolism is disturbed, tissues swell and protein levels decrease. If HDN began to develop early in pregnancy, then everything can end in a miscarriage. If the child still survives, then he will be born very pale, with pronounced edema.
2. Icteric form of HDN. This form is the most common. The main symptoms are the early development of jaundice, anemia, and a significant increase in 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 appeared, the more difficult the HDN will be. Signs of the disease are greenish skin, dark urine and colorless feces.
3. Anemic form of HDN. This form is the most gentle and light. It manifests itself within seven days after the birth of the child. It is not always possible to immediately note the appearance of skin pallor, and therefore HDN can be diagnosed at 2-3 weeks of a baby's life. Outwardly, the child remains the same, but the liver and spleen begin to increase in size. The level of bilirubin will be elevated, but not much. This form of the disease can be easily cured without harmful consequences for the health of the baby.

Diagnosis and treatment of hemolytic disease of the newborn

Antenatal diagnosis is carried out during pregnancy in women who are at risk. If a woman has a negative Rh, then during pregnancy she must undergo three times the presence of antibodies in the blood. It is very important to take into account the results in dynamics, because they can show a high risk of the child's illness. In order to finally make sure of the diagnosis, it is necessary to examine the amniotic fluid for the presence of bilirubin, iron, glucose and protein levels. In addition, suspicions can cause changes in the development of the fetus, which can be detected by ultrasound.

Postnatal diagnosis is carried out after the birth of a child and consists entirely in the study of the clinical symptoms of the disease in a child. At the same time, it is necessary to study absolutely all the data, both in the 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 a critical indicator;
• the level of bilirubin increases every hour by about 6-10 µmol / l;
• there is a severe form of anemia.

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

Prevention of hemolytic disease in a newborn baby

For most people, of greater interest are deficiency anemia, which can occur in almost every person. Therefore, we will dwell in more detail on this type of anemia.

Iron-deficiency anemia- causes, symptoms, diagnosis and treatment

Causes of iron deficiency anemia

Iron deficiency anemia occurs when:

1. lack of iron in the body (premature babies, children under 1 year old, pregnant women)
2. increased need for iron (pregnancy, breastfeeding, period of increased growth)
3. disorders of iron absorption from the gastrointestinal tract and its subsequent transportation
4. chronic blood loss

Clinically, iron deficiency anemia is manifested by three main syndromes - hypoxic, sideropenic and anemic. What are these syndromes? What characterizes each of them? A syndrome is a stable set of symptoms. So, hypoxic syndrome is characterized by shortness of breath, headaches, tinnitus, fatigue, drowsiness and tachycardia; anemic syndrome is expressed in a decrease in the content of the number of erythrocytes and hemoglobin. Sideropenic syndrome is directly related to a decrease in the amount of iron in the body and manifests itself as follows: malnutrition of the skin, nails, hair - skin of an "alabaster" shade, dryness and roughness of the skin, brittle hair and nails. Then the perversion of taste and smell joins (the desire to eat chalk, inhale the smell of washed concrete floors, etc.). There may be complications from the gastrointestinal tract - caries, dysphagia, decreased acidity of gastric juice, involuntary urination (in severe cases), sweating.

Diagnosis of iron deficiency anemia

In the blood, there is a decrease in the content of hemoglobin to 60 - 70 g / l, erythrocytes to 1.5 - 2 T / l, the number of reticulocytes is also reduced or completely absent. Red blood cells of various shapes and sizes appear. The serum iron concentration is below normal.

Treatment of iron deficiency anemia

The treatment of iron deficiency anemia is based on the principles of eliminating the cause of its occurrence - the treatment of diseases of the gastrointestinal tract, as well as the introduction of a balanced diet. The diet should contain foods high in iron (liver, meat, milk, cheese, eggs, cereals, etc.). However, iron preparations are the main means of restoring the amount of iron in the body at the initial stage. In most cases, these drugs are prescribed in the form of tablets. In severe cases, resort to intramuscular or intravenous injections. In the treatment of this anemia, for example, such drugs are used: sorbifer, ferrum-lek, tardiferon, totem and others. The choice of various medicines, including combined ones, is very wide.

When choosing, you should consult with your doctor. Usually, the daily dose for the prevention and treatment of mild anemia is 50-60 mg of iron, for the treatment of moderate anemia - 100-120 mg of iron per day. Treatment of severe anemia is carried out in a hospital and iron preparations are used in the form of injections. Then they switch to tablet forms. Iron preparations cause darkening of the stool, but this is normal in this situation. If an iron preparation causes discomfort in the stomach, then it must be replaced.

Iron refractory anemia causes, symptoms, diagnosis and treatment

Cause of iron refractory anemia

Iron refractory anemia is also called sideroblastic or sideroachristic. Iron refractory anemia develops against the background of normal iron content in the blood serum and a lack of enzymes that are involved in the synthesis of hemoglobin. That is, the main cause of iron refractory anemia is a violation of the processes of "assimilation" of iron.

Symptoms of iron refractory anemia, what is hemosiderosis?

Iron refractory anemia is manifested by shortness of breath, headaches, dizziness, tinnitus, fatigue, drowsiness, sleep disturbances and tachycardia. Due to the high content of iron in the blood, tissues are observed hemosiderosis .Hemosiderosis is the deposition of iron in organs and tissues due to its excess. With hemosiderosis, insufficiency of the cardiovascular system develops due to the deposition of iron in the heart muscle, diabetes mellitus, lung damage, and the size of the liver and spleen increase. The skin becomes earthy.

Diagnosis of iron refractory anemia, what are sideroblasts?

The color index of blood is reduced to 0.6 - 0.4, erythrocytes of various shapes and sizes are present, the amount of hemoglobin and erythrocytes is below normal. There are also changes in the bone marrow - cells appear - sideroblasts. Sideroblasts are cells that have a corolla of iron around the nucleus. Normally, such cells in the bone marrow are 2.0 - 4.6%, and with iron refractory anemia, their number can reach up to 70%.

Treatment of iron refractory anemia

There is currently no treatment that can eliminate it completely. It is possible to use replacement therapy - the infusion of red blood cells and blood substitutes.

B12 deficiency anemia, causes of the disease, diagnosis and treatment.

What is B12? Where is this vitamin found?

First, what is B12? AT 12 is a vitamin that also has the name cyanocobalamin . Cyanocobalamin is found mainly in animal products - meat, liver, kidneys, milk, eggs, cheese. The level of vitamin B12 must be constantly maintained by the use of appropriate foods, since its natural physiological losses occur with feces and bile.

Causes of B12 deficiency anemia

So, B12 deficiency anemia is an anemia that occurs due to vitamin B12 deficiency. A lack of vitamin B12 can be caused by insufficient intake from food or a violation of its absorption in the gastrointestinal tract. Insufficient intake of cyanocobalamin with food is possible in strict vegetarians. Also, a lack of B12 can manifest itself with an increase in the need for it in pregnant women, nursing mothers, and cancer patients. Non-absorption of vitamin B12, supplied with food in sufficient quantities, occurs with diseases of the stomach, small intestine (diverticula, worms) and treatment with anticonvulsants or oral contraceptives.

Symptoms of B12 deficiency anemia

Symptoms of manifestation of B12 - deficiency anemia are characterized by disturbances in the central nervous system and the gastrointestinal tract. So, consider these two large groups of symptoms:

1. from the central nervous system. There is a decrease in reflexes, paresthesia (“goosebumps”), numbness of the limbs, a feeling of cottony legs, gait disturbance, memory loss
2. from the gastrointestinal tract. There is an increased sensitivity to acidic foods, glossitis, difficulty swallowing, atrophy of the gastric mucosa, an increase in the size of the liver and spleen

In the blood system, there is a transition to the megaloblastic type of hematopoiesis. This means that giant erythrocytes with a shortened life span, brightly colored erythrocytes without enlightenment in the center, pear-shaped and oval erythrocytes with Jolly bodies and Kabo rings appear in the blood. Giant neutrophils also appear, the number of eosinophils (up to complete absence), basophils and the total number of leukocytes decreases. In the blood, the concentration of bilirubin is increased, and therefore, slight yellowness of the skin and sclera of the eyes can be observed.

Treatment of B12 deficiency anemia

First of all, it is necessary to cure diseases of the gastrointestinal tract and establish a balanced diet, with a sufficient content of vitamin B12. The use of a course of vitamin B12 injections quickly normalizes hematopoiesis in the bone marrow, and then a constant, regular intake of a sufficient amount of vitamin B12 with food is necessary.

Folate deficiency anemia, causes, symptoms and treatment

Symptoms of folate deficiency anemia

With folic deficiency anemia, the gastrointestinal tract suffers, therefore, the manifestations of this anemia are associated with disorders of the gastrointestinal tract. There is an appearance of hypersensitivity to acidic foods, glossitis, swallowing difficulties, atrophy of the gastric mucosa, an increase in the size of the liver and spleen.
In the blood system, the same changes occur as in B12 deficiency anemia. This is a transition to the megaloblastic type of hematopoiesis, the appearance of giant neutrophils, a decrease in the number of eosinophils, basophils and the total number of leukocytes.

Treatment of folate deficiency anemia

To treat this type of anemia, folic acid tablets are used and the diet is normalized, in which there should be foods containing a sufficient amount of folic acid.

Hypoplastic anemia, causes, diagnosis, treatment

Symptoms of hypoplastic anemia

Hypoplastic anemia can be hereditary or acquired, but all subtypes of this type of anemia are characterized by the same manifestations. Consider these symptoms:

1. Bleeding, bleeding gums, fragility of blood vessels, bruising on the skin, etc. These phenomena occur due to the low content of platelets in the blood.
2. Ulcerative - necrotic lesions of the mouth, pharynx, nose, skin. Accession of infections. This is due to the low number of white blood cells in the blood.
3. Dizziness, headaches, tinnitus, drowsiness, fatigue, fainting, sleep disturbances, shortness of breath, heart palpitations, etc.
4. In the general blood test, a decrease in the content of all blood cells - erythrocytes, leukocytes, platelets. In the bone marrow, there is a picture of desolation, since the foci of hematopoiesis are replaced by adipose tissue.

What causes can cause such damage to the bone marrow? Hereditary anemia, respectively, is inherited, but acquired? All factors that can lead to the development of hypoplastic anemia are divided into exogenous (external) and endogenous (internal). The table shows the main exogenous and endogenous causes that can cause the development of hypoplastic anemia.

Treatment of hypoplastic anemia is strictly within the competence of a hematologist. Various methods of stimulating hematopoiesis, or bone marrow transplantation, can be used.

So, we have considered all the main types of anemia. Of course, there are many more of them, but we cannot embrace the immensity. If any signs of anemia appear, you should consult a doctor in a timely manner. And regularly take a blood test for hemoglobin.

Hemolytic disease of the newborn (HDN)- a disease caused by the incompatibility of the blood of the mother and the fetus for various antigens that are present in the blood of the latter (inherited from the father) and absent in the blood of the mother. Most often, the disease develops when the blood of the mother and fetus is incompatible with the Rh antigen (1 case per 200-250 births). It should be noted that there are several types of Rh antigen, designated according to Wiener - Rh 0, Rh ", Rh". At the suggestion of Fisher-Reiss, the types of the Rh antigen began to be designated respectively by the letters D, E and C. Usually, the Rh conflict develops with incompatibility for Rh 0, i.e. (D) antigen, for other types - less often. The cause of hemolytic disease may also be incompatibility for antigens of the ABO system.

Hemolytic disease of the newborn is possible when there is a mismatch between the blood of the mother and the fetus and other antigens: M, N, S, P or systems Lutheran (Lu), Levi (L), Kell (Kell), Dufy (Fy), etc.

Pathogenesis. If the blood of the mother and fetus does not match, antibodies are produced in the body of a pregnant woman, which then penetrate during pregnancy through the placental barrier into the blood of the fetus and cause destruction (hemolysis) of its red blood cells. As a result of increased hemolysis, a violation of bilirubin metabolism occurs. Violation of the latter contributes to liver failure in the form of immaturity of the glucuronyltransferase enzyme system. The latter is responsible for the conjugation of indirect bilirubin with glucuronic acid and its transformation into non-toxic direct bilirubin (bilirubin-glucuronide).

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

1. during pregnancy, which leads to congenital forms of HDN (the birth of macerated fetuses, edematous, anemic, icteric forms);
2. during childbirth, which leads to the development of postpartum icteric form;

Anti-Rh antibodies are formed in 3-5% of women with Rh-negative blood during pregnancy with a fetus with Rh-positive blood. Usually children with Rh conflict are born with HDN from the 2nd-3rd pregnancy, less often from the 1st pregnancy in cases of sensitization in the past by blood transfusions without taking into account the Rh factor. In some women, antibodies may be low and antibodies do not cross the placenta, and an Rh-sensitized woman may have a healthy Rh-positive baby after giving birth to children with HDN. With ABO incompatibility, the disease develops already during the 1st pregnancy.

The severity of HDN is not the same, it depends on the amount of antibodies that have penetrated from the mother to the fetus, the compensatory capabilities of the fetal body. Hemolytic disease of the newborn manifests itself in 3 main forms: anemic, icteric, edematous.

Clinic. Hemolytic disease of the newborn can manifest itself in the following ways:

1. the child dies during fetal development (on the 20-30th week);
2. born with universal edema;
3. in the form of early onset severe jaundice or
4. severe anemia.

Common symptoms for all forms of the disease are normochromic anemia of a hyperregenerative nature with the presence in the blood of young forms of erythrocytes (erythroblasts, normoblasts, an increased number of reticulocytes), enlargement of the liver and spleen.

edematous form the disease develops with prolonged action of isoantibodies during pregnancy; the fetus does not die, since toxic products are excreted through the placenta into the mother's body. Due to the adaptive reactions of the fetus, foci of extramedullary hematopoiesis are formed, the spleen (5-12 times), liver, heart, endocrine glands increase. Liver functions are disturbed, especially protein-forming, vascular permeability increases, hypoalbuminemia develops. All this leads to pronounced edema of the subcutaneous fat layer, accumulation of fluid in the cavities (pleural, abdominal) and an increase in fetal weight by almost 2 times against the age norm. Anemia (Hb 35-50 g/l, erythrocytes 1-1.5 x 10 12 /l), erythroblastemia are pronounced. The placenta is sharply enlarged, edematous. Metabolic disorders in some cases can cause fetal death before birth or during childbirth. The edematous form is characterized by an extremely severe course and in most cases ends in death. A child born alive dies within minutes or hours.

Currently, some children with generalized congenital edema can be saved by the careful use of exchange transfusions.

icteric form develops under the influence of isoantibodies on a sufficiently mature fetus. The baby is usually born at term, with a normal body weight, with no visible changes in skin color. HDN develops a few hours after birth. Already on the 1st-2nd day of his life, jaundice is detected, which is rapidly increasing; less often a child is born with icteric coloration of the skin. Amniotic fluid and primordial lubrication have the same color. All children with the icteric form of the disease have an increase in the liver, spleen, lymph nodes, and sometimes the heart; an increase in the content of bilirubin in the umbilical cord blood - above 51 µmol / l (in healthy newborns it ranges from 10.2-51 µmol / l, averaging 28.05 µmol / l according to Van den Berg). In the next 72 hours in children with HDN, the level of bilirubin increases rapidly, the hourly increase is from 0.85 to 3.4 µmol/l.

You can determine the hourly increase in bilirubin using the formula:

The immaturity of the enzyme systems of the liver of a newborn leads to the accumulation of indirect bilirubin in the blood. Indirect bilirubin is a cytoplasmic poison and causes damage to hepatocytes (liver cells), myocardial muscle cells, but especially neurons (nerve cells).

An intensive increase in the content of indirect bilirubin (an hourly increase from 0.85 to 3.4 μmol / l), if measures are not taken to reduce it, quite soon (after 24-48 hours) leads to its excessive accumulation and the appearance of pronounced jaundice in the child with symptoms of bilirubin intoxication and damage to the central nervous system (nuclear jaundice, or bilirubin encephalopathy), which is accompanied by a deterioration in the child's condition: lethargy appears, the child sucks worse, frequent regurgitation, vomiting appear, tonic convulsions are often noted (on the 4-5th day of life ), stiff neck, oculomotor disorders and spasms of gaze (a symptom of the "setting sun" is an involuntary downward turn of the eyeballs, in connection with which a strip of sclera is visible between the upper edge of the cornea and the upper eyelid); breathing becomes slow and irregular, bouts of cyanosis develop, congenital reflexes of Moreau, Robinson, Babkin decrease. In addition, there is a deposition of crystalline bilirubin in the medulla of the kidneys - a bilirubin infarction of the kidneys develops. Impaired liver function in HDN is manifested not only by a violation of the formation of direct bilirubin, but also by a decrease in the synthesis of prothrombin and protein. The level of prothrombin in the blood decreases. Bleeding time is increased. Loading the liver with hemolysis products often leads to a violation of the excretion phase with the development of obstructive jaundice - the so-called bile thickening syndrome. In this syndrome, the feces are discolored (usually in children with this form of feces are bright yellow), the liver is even more enlarged, the level of direct bilirubin in the blood rises, there are a lot of bile pigments in the urine (Gmelin's reaction is positive).

The toxic properties of indirect bilirubin begin to appear when it is not bound to plasma albumin (the bilirubin-binding ability of blood plasma is reduced) and therefore easily penetrates beyond the vascular bed. With a sufficient amount of albumin in the blood, brain damage begins to develop at a bilirubin level that is significantly higher than the critical one.

The danger of damage to the central nervous system in the form of bilirubin intoxication (nuclear jaundice) appears with an increase in the level of indirect bilirubin in a full-term baby above 306-340, in a premature baby - from 170 to 204 µmol / l. The resulting bilirubin encephalopathy can be fatal as early as 36 hours after the birth of a child. Children who remain alive are significantly behind in mental development.

In the future, there is a moderate delay in the overall development of the child. Due to the suppression of immune defense mechanisms, such children easily develop pneumonia, omphalitis, and sepsis. Bilirubin intoxication, complications of infectious diseases, anemia, changes in the internal organs cause a severe course of congenital icteric form of HDN with a large number of deaths. Timely treatment of patients can prevent adverse outcomes of this form of HDN.

anemic form proceeds relatively easily. It develops as a result of a short exposure of a small dose of maternal isoantibodies to the fetus; at the same time, the damage to the fetus is small, the products of hemolysis are discharged by the placenta into the mother's body. After birth and cessation of placental function, with sufficient liver function, there is no jaundice, the child develops normally in the presence of anemia. These cases are rare. The main symptom of this form of the disease is the pallor of the skin in combination with a low amount of hemoglobin and erythrocytes, an increase in immature forms of erythrocytes (erythroblasts, normoblasts, reticulocytes). The liver and spleen are enlarged. Anemia develops at the end of the 1st - beginning of the 2nd week of life, the content of hemoglobin and erythrocytes decreases, anisocytosis, polychromasia, erythroblastosis appear. The liver and spleen are enlarged.

Usually, the pallor of the skin is clearly detected from the first days of life, but in milder cases it is masked by physiological erythema and transient jaundice and is clearly detected only by the 7-10th day of life. With fractional transfusions of Rh-negative blood, the child recovers quickly.

The development of hemolytic disease of the newborn is not always determined by the height of the titer of isoimmune antibodies in pregnant women. The degree of maturity of the body of the newborn matters - a more severe course of the disease is noted in premature babies.

Hemolytic disease of the newborn, associated with the incompatibility of the blood of the mother and child according to the antigens of the ABO system, occurs with the same frequency as HDN, due to Rh incompatibility. HDN associated with group incompatibility occurs when the mother has 0 (I) blood type, and the child is A (II) or B (III). Usually the disease occurs during the 1st pregnancy. Clinically, hemolytic disease of the newborn associated with ABO incompatibility proceeds in a mild form (in 90% of cases), resembling transient jaundice along the way. However, with a frequency of one case per 2000-2200 births, the disease can proceed in the form of severe jaundice and be complicated by bilirubin encephalopathy if active measures are not taken in a timely manner to reduce the level of bilirubin, including exchange transfusion.

The cause of the severe course of the process in such cases is concomitant acute and chronic diseases of the mother during pregnancy, causing an increase in the permeability of the placental barrier for isoantibodies. HDN associated with group incompatibility is not observed in the form of edema.

Early diagnosis. Allocate pregnancy, "threatened" by the development of hemolytic disease in the fetus. The assumption about the possibility of developing HDN should arise when examining a pregnant woman in a antenatal clinic. Rh-negative blood in the mother and Rh-positive in the father, indications in the anamnesis of the mother for blood transfusion without taking into account the Rh factor should raise the possibility of HDN in the unborn child. The presence of a aggravated anamnesis (stillbirth, spontaneous miscarriages, the birth of infants with HDN, a lag in the mental development of children from previous pregnancies) makes us think about the possibility of a severe course of HDN in the expected child and taking such a woman into special account with the need to conduct a complex of special studies. First of all, the blood of a woman with a Rh-negative affiliation should be examined for the presence of Rh antibodies: if the latter are detected, preventive measures should be taken to reduce the effects of isoimmunization.

The diagnosis of a disease in an intrauterine fetus can be established on the basis of the results of a study of amniotic fluid obtained using amniocentesis (their optical density, their bilirubin content).

It is important to establish a diagnosis of HDN with an assessment of the severity of the disease immediately after the birth of the child. The criteria for the presence of the disease are: Rh-negative blood of the mother and Rh-positive blood in a newborn with the presence of Rh antibodies in the blood of the mother; with group incompatibility - the presence of group 0 (I) in the mother and A (II) or B (III) - in the child with the determination in the mother's blood serum of a high titer of isoimmune α- or β-agglutinins in the protein medium.

Table 1. Differential diagnostic symptoms in Rh- and AB0-incompatibility

As a rule, in the case of an extremely severe course of HDN, the diagnosis does not cause difficulties even in the absence of anamnestic data; amniotic fluid and labor lubrication are yellow or green, the child is edematous, icteric or pale, the liver and spleen are significantly enlarged.

In cases where the condition is unclear, for early diagnosis and prognosis of the disease, a clinical analysis of the blood of the newborn, especially the umbilical cord, is important, since changes in it with HDN are detected much earlier than other clinical signs of the disease.

The following indicators of umbilical cord blood indicate the presence of HDN:

1. hemoglobin below 166 g/l;
2. the presence of erythroblasts and normoblasts in an amount of more than 10 per 100 leukocytes;
3. positive Coombs test with Rh-conflict; with a conflict in the ABO system, the Coombs test is negative;
4. the content of bilirubin is above 51 μmol / l according to Van den Berg;
5. a decrease in the level of blood protein to 40-50 g / l.

If cord blood was not taken for research, then if there is a suspicion of the presence of hemolytic disease due to the early onset of jaundice (on the first day after birth), it is necessary to assess the severity of hemolytic disease according to the hourly increase in bilirubin.

It is difficult to make an early diagnosis in cases where TTH is caused by other antigens. To do this, a study of the mother's blood serum for the presence of antibodies to rare antigens is carried out. While the cause of the disease is being clarified, treatment should be aimed at combating intoxication with indirect bilirubin.

Differential Diagnosis. In the differential diagnostic relation, one should mainly bear in mind hyperbilirubinemia with an increase in indirect bilirubin and hyperbilirubinemia, in which there is hemolysis, i.e., which occur with erythroblastosis and reticulosis in the peripheral blood:

• due to congenital or acquired defects of the erythrocyte membrane with typical changes in their morphology, such as spherocytosis, elliptocytosis, stomatocytosis and pycnocytosis;
• as a result of enzymatic defects in erythrocytes - glucose-6-phosphate dehydrogenase (the most common enzymatic-metabolic disease), pyruvate kinase, etc.

The main differential diagnostic criteria are positive Coombs or Munch-Andersen tests for hemolytic disease of the newborn and proof of enzyme deficiency. These include thalassemia and disseminated intravascular coagulopathy. To confirm the diagnosis of alpha thalassemia, the family history of the child is important and, mainly, the establishment of Barth's hemoglobin by means of hemoglobin electrophoresis. The diagnosis of disseminated intravascular coagulopathy is facilitated by characteristic changes in blood coagulation factors or global tests, such as prothrombin time, thrombin, heparin time, platelet count, fragmented erythrocytes.

Less well known and more difficult to diagnose are metabolic endocrine hyperbilirubinemias. Crigler-Najjar syndrome (familial non-hemolytic hyperbilirubinemia with kernicterus) is characterized by indirect hyperbilirubinemia without evidence of hemolysis and is transmitted as an autosomal recessive disease. Parents have a reduced ability to conjugate bilirubin without jaundice. Jaundice in a child appears already in the first days after birth, sometimes with very high values ​​of bilirubin. In this regard, there may be a need for an exchange transfusion of blood.

Transient familial neonatal hyperbilirubinemia or Lucey-Driscoll syndrome manifests as an increase in indirect bilirubin without evidence of hemolysis. It is believed that it occurs under the influence of the inhibitory effect of some factor, in all likelihood, a steroid in pregnant women, which disrupts the normal conjugation of bilirubin. With severe jaundice in some children, an exchange transfusion of blood is necessary.

Jaundice regularly accompanies neonatal hypothyroidism with its characteristic appearance, hypotension, rough voice, large abdomen, and generally delayed development of the bone nuclei and specific abnormalities in the level of thyroid hormones. In children, indirect hyperbilirubinemia is seen in newborns with hypopituitarism or anencephaly. Pronounced jaundice in these two groups of diseases is associated with the presence of hypothyroidism.

Many drugs, hormones and other substances and conditions play a role in the development of hyperbilirubinemia in newborns, such as sulfonamides, vitamin K, especially in high doses, novobiocin, hypoxia, acidosis, etc. Three α-20-β-pregnadiol and the milk of some mothers is also the cause of this painful condition.

In newborns whose mothers are sick with diabetes mellitus, hyperbilirubinemia with an increase in indirect bilirubin without hemolysis is observed more often and is more pronounced than in healthy newborns. It appears by the 3rd day after birth, when the hematocrit also rises, which currently explains the hyperbilirubinemia in these children.

Jaundice and anemia can be observed with sepsis, cytomegaly, toxoplasmosis, congenital infectious hepatitis, syphilis and other diseases.

Treatment of HDN- complex, aimed at the fastest removal of toxic products of hemolysis from the body of a newborn, mainly indirect bilirubin, as well as antibodies that contribute to the continuation of the hemolytic process, and to increase the functional capacity of various systems and organs, especially the liver and kidneys.

The most effective method of combating hyperbilirubinemia in severe and moderate forms of the disease is early exchange blood transfusion at the rate of 150-180 ml/kg of newborn weight. In case of a Rh-conflict, one-group Rh-negative blood is transfused, in case of an ABO-conflict, erythrocytes of the 0 (I) group, suspended in the plasma of the AB (IV) group, are transfused. For exchange transfusion, the donor's blood (stabilizers 7, 5) must be fresh, no more than 3 days of storage after collection.

The indication for exchange transfusion is:

• an increase in the content of bilirubin in the blood plasma on the first day to 171.04 µmol/l
• an increase in bilirubin in the blood by 0.85 µmol / l per hour

Early applied exchange transfusion allows correcting anemia, removing a significant part of sensitized erythrocytes, which, in turn, limits the development of the hemolytic process and eliminates a certain amount of bilirubin before it is distributed in larger quantities in the extravascular space. In the presence of severe anemia (hematocrit 35% or less), an exchange transfusion is used - 25-80 mg / kg body weight of erythrocyte mass 30 minutes after birth in order to increase the hematocrit to 40%. The possibility of hypovolemia in such children is indicated. Therefore, it is recommended that before proceeding with manipulations in order to change blood volume, a thorough measurement of venous and arterial pressure should be carried out.

The most expedient and technically easy to perform is an exchange transfusion through the umbilical vein (the first 3-5 days of life). First, 10 ml of blood is released through the catheter inserted into the umbilical vein, then the same amount of donor blood is injected, the duration of the procedure is 1 ½ - 2 hours (the speed of the blood replacement operation is 2-3 ml / min), at the end of the transfusion, it is injected for 50 ml of blood is more than is excreted. After replacing every 100 ml of blood, the child must be injected intravenously with 1 ml of a 10% solution of calcium chloride. After blood transfusion, detoxification therapy is carried out: abundant fluid intake, intravenous transfusion of plasma, albumin, glucose (100-250 ml).

Due to the fact that the citric acid of banked blood for exchange transfusion is very quickly metabolized in the liver to bicarbonates, most children have no difficulty during the transfusion itself without alkalinization, if it is done very slowly. However, after transfusion, some newborns develop alkalosis, which can last for 72 hours. It is dangerous to infuse acid-preserved blood, as this can directly affect the myocardium and cause cardiac arrest. In this regard, in children in a state of shock or significant metabolic acidosis, it is recommended to use alkalized blood. On the other hand, it should not be forgotten that with the introduction of alkalizing agents there is a danger of an increase in osmolarity with its consequences. Elimination of 60 ml of plasma from a donor's blood prior to exchange transfusion reduces acidity and citrate load and normalizes hematocrit.

Some authors recommend using heparinized blood for exchange transfusion. It should be noted that the content of ionized calcium, electrolytes, acid-base balance and blood sugar levels do not change. But as a consequence, the use of heparin significantly increases the level of non-esterified fatty acids, which can replace bilirubin in the albumin-bilirubin complex. It should also be borne in mind the possible changes in the coagulation parameters of the newborn. The most important disadvantage of heparinized blood when used for exchange transfusion is that it should be used no later than 24 hours from the moment it is taken from the donor and preserved.

It follows from the foregoing that exchange transfusion of blood in newborns is associated with a number of complications, if we do not take into account the biochemical changes that may occur during this manipulation.

Phenobarbital is used to improve liver function. Treatment with phenobarbital is due to its inducing effect on the activity of glucuronyl transferase and the established increased ability of ligandin to bind bilirubin in the hepatocyte. It is used from the first or second day at a dose of 5 mg/kg of body weight 2-3 times a day, some clinicians recommend up to 10 mg/kg of body weight per day. Consider that this treatment cannot give result at already shown jaundice.

In case of violation of the bilirubin excretory function of the liver and the development of "bile thickening syndrome", a 5-10% solution of magnesium sulfate 5 ml 2-3 times a day, 10-20% solution of xylitol, holosas, sorbitol can be administered orally. Duodenal sounding for the purpose of bile drainage is also effective. However, treatment with agar, activated charcoal and magnesium sulfate to reduce enterohepatic circulation and resorption of bilirubin is rejected by most authors on the basis of daily practice, since it does not give positive results.

The child is prescribed: feeding with donor milk, breastfeeding not earlier than the 10th-12th (according to indications and later) days of life, adenosytrophosphoric acid (ATP) 0.5 ml intramuscularly, methionine, ascorbic acid, pyridoxine, cyanocobalamin, tocopherol 10 each mg by mouth. Inside, prednisolone is also prescribed at 1-1.5 mg / kg for 7-8 days.

Phototherapy is also shown (irradiation of newborns with lamps of "blue or blue" light): sessions of 3 hours at intervals of 1-2 hours, i.e. up to 12-16 hours a day (phototherapy takes from 2 to 6 days). Under the action of light, bilirubin is oxidized, turning into biliverdin and other non-toxic substances.

Currently, phototherapy is the most appropriate method for regulating bilirubin levels in newborns. Statistics show that after the introduction of phototherapy into practice, the number of exchange transfusions has decreased significantly. The method is based on the photoisomerization of bilirubin-IX-α and the production of photobilirubin, which is very quickly excreted in the bile. This process takes place in the skin and its capillary network at a depth of 2 mm. The indications for this treatment are mainly hyperbilirubinemia of prematurity with Rh- and ABO-incompatibility, usually after exchange transfusion. There are reports of a more favorable effect of phototherapy than exchange transfusion in a newborn with non-hemolytic hyperbilirubinemia. The indications for turning on phototherapy are shown in Table 1. 2, in which each individual case is scored according to postnatal age, birth weight, birth pathology, and bilirubin level.

In the presence of perinatal hypoxia, respiratory distress, metabolic acidosis (pH 7.25 or below), hypothermia (below 35°C), low serum protein (50 g/l and below), cerebral impairment, birth weight less than 1500 g, and symptoms clinical deterioration, phototherapy and exchange transfusion should be used, as in the subsequent, higher bilirubin group indicated in Table 2.

Table 2. The main directions in the treatment of hyperbilirubinemia (according to Brown et al.)

However, with longer use, phototherapy leads to a number of side effects: retinal damage, embryogenesis deviations (experiments on animals), thrombocytopenia, pallor of the skin and the "copper child" syndrome observed with data indicating holostasis. It is hypothesized that the retention of some phototherapy product is the cause of this particular skin color in the child. As side effects, the presence of green feces and the loss of fluids and some salts with feces are also described.

In practice, the following precautions should be taken into account:

• Before using phototherapy, the etiology of hyperbilirubinemia should be determined, if possible, in order to avoid missing a life-threatening condition.
• Protect eyes and gonads
• Monitor baby's temperature
• Control the water balance (twice a day, measure the child's temperature, amount and specific gravity of urine, hematocrit) and, if necessary, introduce more liquid
• Examine bilirubin every 12 hours, and more often if indicated, without relying on an assessment of the severity of jaundice by skin color
• Control platelet count
• Examine hematocrit, especially in hemolytic disease
• Use a lactose-free nutrient mixture for dyspeptic feces containing an increased amount of reducing substances

The issue of repeated replacement blood transfusions is decided by the rate of increase in the level of bilirubin in dynamics. In full-term newborns, such indications occur with an hourly increase in bilirubin content of more than 5.13 μmol / l, or one should focus on the level of bilirubin, which exceeds critical numbers (according to the Polachek scale): the level of indirect bilirubin in full-term infants is over 306 and in premature infants - over 204 μmol / l.

With the development of anemia in a child (decrease in hemoglobin below 80 g / l), anti-anemic treatment is carried out by fractional blood transfusions of 20-25 ml 2-3 times. Children with HDN need careful care, proper feeding.

If the child has not received an exchange transfusion, then it is necessary to feed him with donor milk for the first 2-3 weeks, focusing not only on the content of Rh antibodies in the mother's milk, but also on the severity of the disease.

Children treated with blood exchange transfusions can be fed with mother's milk at an earlier date (from the 5-7th day of life).

After treatment in the acute period of the disease, upon discharge from the maternity hospital or hospital, the child needs to do a blood test every 10-14 days from 3 weeks of age to 2 months and, if hemoglobin decreases, take a course of treatment with vitamin B 12, 50 mcg every other day, 10 -12 injections per course. Children with damage to the central nervous system are prescribed a course of vitamin B 12 - 50 mcg every other day, for a course of 20 injections.

Forecast. Children who have had hemolytic disease of the newborn and are promptly treated with sufficient volume of exchange transfusions usually develop well in the future. In mild and moderate forms of jaundice, the prognosis is favorable. Patients with HDN in the form of severe jaundice with hyperbilirubinemia above the "critical" numbers in the acute period, not treated in a timely manner by exchange transfusions, may die during the first days of life. In the survivors, during the development in the acute period of nuclear jaundice, an organic lesion of the central nervous system is later detected, which is manifested by a lag in physical and mental development, hearing loss and speech impairment.

Children with residual effects in the state of the central nervous system need restorative therapy. They should be well cared for, massaged, prescribed drug therapy - glutamic acid, vitamins of the B complex (B 6, B 1, B 12), aminalon.

Preventive actions to prevent HDN or reduce its severity should be carried out already in the antenatal clinic and are as follows:

1. Determination of the Rh factor and blood type in all pregnant women
2. All women with Rh-negative blood and with the 0 (I) group must be registered, a detailed anamnesis should be collected from them, and it should be found out if they have had a blood transfusion in the past without taking into account the Rh factor. In all these women, it is necessary to determine the titer of Rh antibodies regularly (once a month). With an unfavorable (according to HDN) history, a high titer of antibodies, an early (2 weeks) delivery is performed.
3. At present, desensitization with Rh-negative blood is successfully carried out through a number of special measures: in the last 3 months of pregnancy, this is the grafting of a skin flap from the husband, the introduction of a primigravida (if the child has Rh-positive blood) immediately after birth (during the first 72 hours after birth) anti-Rh-gamma-immunoglobulin (200-250 mcg), prepared from the blood of Rh-negative women who gave birth to a Rh-positive child. In this way, the goal is to neutralize the Rh factor as an antigen.
4. Pregnant women with Rh-negative blood, who have a rapidly increasing antibody titer, especially if previous pregnancies ended unsuccessfully, should be placed in a specialized maternity hospital 3-4 weeks before delivery to monitor the course of pregnancy. In pregnant women with a high titer of antibodies who are in the hospital, it is necessary to monitor the dynamics of the level of bilirubin in the fetus. With high titers of bilirubin, an earlier delivery may be necessary if the optimal degree of fetal maturity (which is possible with modern studies) is ascertained, allowing it to cope with extrauterine life. Cases of intrauterine exchange transfusion of blood in the fetus are described.
5. With Rh-negative blood, it is necessary to maintain the first pregnancy, since usually the first child is born normal, the threat of HDN in the children of such women increases with repeated pregnancies.

Anemia in newborns is a condition that is characterized by a decrease in hemoglobin levels and a violation of the main functions of red blood cells. In infants, this condition deserves special attention, since they are not able to fully compensate for the lack of oxygen. This can negatively affect the development of the child's nervous system in the future, the functioning of the heart and all internal organs, leading to long-term consequences, some of which may be irreversible.

ICD-10 code

D50 Iron deficiency anemia

P55 Hemolytic disease of the fetus and newborn

Epidemiology

Statistics on the spread of anemia suggests that about 5% of newborn babies encounter this problem in the first month of life, and more than 40% of cases of anemia are etiologically associated with problems of pregnancy and childbirth. The prevalence of iron deficiency anemia ranges from 0.9 to 4.4%, depending on race, ethnicity, and socioeconomic status, but represents only about 40% of the total anemia in young children. The remaining 60% are hemolytic and aplastic anemia.

Causes of anemia in a newborn

Most of the anemias encountered today are anemias associated with iron deficiency. Other anemias are congenital aplastic ones, hemolytic ones also take place, but much less often and with a more vivid clinical picture.

To understand the causes of anemia in newborn babies, you need to consider the role of iron in the blood. If we simplify the scheme, we can imagine that iron is in the center of the heme molecule, which is externally surrounded by the protein globin. This is how hemoglobin itself is built, which is the basis for an erythrocyte. It is hemoglobin that is responsible for binding the oxygen molecule in the lungs and transporting such a complex throughout the body, to every cell that requires oxygen. With a decrease in iron levels, the level of heme also decreases, so red blood cells cannot bind oxygen, which underlies the development of anemia and its manifestations. That is why it is so important for a newborn baby that the mother, and then the child, have enough iron.

Sufficient level of iron - a condition in which the iron content is sufficient to maintain normal physiological functions, in this case, a pregnant woman should take into account the double need for it.

Iron deficiency is a condition in which the iron content is insufficient to maintain normal physiological functions. Iron deficiency is the result of insufficient iron absorption to meet the increased needs of the mother during pregnancy, or is the result of a long-term negative iron balance. Either of these situations leads to a decrease in iron stores, which is determined by measuring the concentration of ferritin in the blood serum or the iron content in the bone marrow. Therefore, iron deficiency in a mother during pregnancy is the first and main cause of iron deficiency anemia in a newborn, even regardless of the gestational age.

The deficiency of total iron in the body in premature infants is greater, the lower the gestational age. It is exacerbated by rapid postnatal growth, which occurs in many children, and by frequent phlebotomies without adequate blood replacement.

Of the iron present in the body of a newborn, 80% accumulates during the third trimester of pregnancy. Babies born prematurely lose this rapid growth period and are deficient in total body iron. A number of maternal conditions, such as anemia, hypertension with intrauterine growth restriction, or diabetes during pregnancy, can also lead to decreased fetal iron stores in both term and preterm infants.

The concept of breastfeeding is very related to this, since breast milk contains as much iron as the baby needs in his first five months of life. And if the baby does not breastfeed immediately after birth, then this can be one of the main reasons for the development of anemia in him.

Among other causes of anemia in a newborn that may be associated with pregnancy and childbirth, pathology of the intranatal period can be attributed. Fetoplacental transfusion and intranatal bleeding due to birth trauma and anomalies in the development of the vessels of the placenta and umbilical cord can lead to significant blood loss in the mother. This continuously affects the formation of red blood cells in the child.

Anemia can also develop for other reasons, which are more serious and are associated with the pathology of iron intake into the body of the newborn due to organic pathology. Violation of iron absorption can be observed in malabsorption syndrome, congenital intestinal obstruction, short bowel syndrome. All this leads to the development of anemia. Iron loss in significant amounts can be observed during bleeding of various etiologies. In newborns, this is most often bleeding from the navel or intestinal bleeding with hemorrhagic disease.

Although iron deficiency is the main cause of anemia, you should not forget about other anemias that a newborn may have. These include congenital aplastic anemia and hemolytic.

Aplastic anemia is a condition that is characterized by a decrease in hemoglobin levels due to a violation of the formation of red blood cells in the bone marrow. In newborns, aplastic anemia is more often congenital. The main cause of congenital aplastic anemia can never be established with certainty. Children are born already with pathology, and the exact cause cannot be established. Risk factors include ionizing radiation, genetic mutations, drugs, viral and bacterial agents, and more.

At the heart of the pathogenesis of the development of aplastic anemia is a violation of the development of the stem cell, which gives rise to all blood cells. And depending on which germ is involved, there may be a decrease in the level of other blood cells.

Hemolytic anemia occurs in a child more often due to hereditary causes. This is due to a mutation of the gene that is responsible for the structure of the erythrocyte cell. Therefore, its membrane cannot function normally and periodically it is destroyed, which is called hemolysis. Minkowski-Choffard anemia is most common in newborns. This anemia is due to a genetic mutation of the erythrocyte membrane proteins spectrin and ankyrin. Therefore, the main cause of anemia in this disease is a violation of the cell membrane due to a lack of these proteins.

Anemia in newborns have similar clinical manifestations, but it is imperative to know the cause and understand the pathogenesis of development for the correct treatment tactics.

Symptoms of anemia in a newborn

Speaking about the clinical manifestations of anemia, you need to understand the stages of its development. If we are talking about iron deficiency anemia, then it has its own stages of development. First, the baby is born absolutely healthy, because immediately after birth he has a physiological increase in the level of red blood cells. But at this time, the number of red blood cells that should be formed in the bone marrow decreases due to lack of iron. This corresponds to the latent or latent stage of anemia. At the same time, there are no clinical manifestations yet, but a lack of iron leads to a critical decrease in hemoglobin and red blood cells.

The next stage is a long-term iron deficiency leading to clinical symptoms, so this is a clear stage of anemia.

Symptoms of anemia in a newborn baby are very difficult to identify, especially for the mother. Since the child is still very small and sleeps most of the time, the mother fails to notice any signs. It is also common for a child to develop physiological jaundice, which can make it difficult to see symptoms. This proves the importance of preventive examinations of the child during this period.

The first signs of anemia differ, depending on the etiology. Iron deficiency anemia in newborns is the most common, and its first symptom is the pallor of the skin and mucous membranes of the child. All newborn babies are usually red at first, and then pink, and with anemia they are a little pale. This symptom is highly subjective, but it may be the first sign of anemia.

Other clinical manifestations may already be associated with severe hypoxia caused by a lack of oxygen. This may be the appearance of cyanosis of the skin and shortness of breath during feeding, the anxiety of the baby.

All symptoms of anemia can be summarized and divided into several groups. The main syndromes for anemia in newborns are anemic-hypoxic and sideropenic, and speaking of hemolytic anemia, hyperbilirubinemia syndrome is also added.

The first syndrome occurs due to a lack of oxygen and is manifested by pallor, especially mucous membranes, poor health, decreased appetite, and lack of strength. All this in a child is manifested by the fact that he eats poorly and does not gain weight. Sideropenic syndrome occurs due to a malfunction of enzymes that depend on oxygen. This disrupts the work of all cells and is manifested by dry skin against the background of pallor, in newborns the fontanel is poorly overgrown, there is no muscle hypertonicity inherent in them, but on the contrary, hypotension occurs.

Hemolysis syndrome occurs due to increased breakdown of red blood cells in the vascular bed, which causes the release of bilirubin and an increase in its concentration. Then, against the background of anemia and all of the above symptoms, a yellow coloration of the child's skin and sclera occurs. Hemolytic anemia in a newborn is most often genetic in nature. One of the types of such pathology is Minkowski-Choffard anemia. One of the family members has this disease, which simplifies the diagnosis a bit. All syndromes are the same, and it is important not to confuse jaundice with such hemolytic anemia with physiological.

Congenital anemia in newborns is more often aplastic in nature and is the most severe type of anemia. There are several types. One of them is Blackfan-Diamond anemia. With this pathology, it is the number of red blood cells that decreases due to the defeat of this germ in the red bone marrow. In the first month of life, it rarely sheds, clinical signs are more visible closer to the sixth month of life.

Congenital Estrane-Dameshek anemia is a decrease in the level of all bone marrow cells. Therefore, in addition to anemia and hypoxia, there will be bleeding and early infectious lesions. Another type of aplastic congenital anemia is Fanconi anemia. The symptoms of this disease, in addition to anemic, are congenital malformations in the form of microcephaly, other malformations of the skull, underdevelopment of fingers, underdevelopment of internal organs.

It is also necessary to highlight conditions in which a decrease in the amount of hemoglobin can also be observed - this is anemia in premature newborns. This is caused by the immaturity of the bone marrow and unpreparedness for the processes of breathing through the lungs. This is considered normal and such anemia may resolve on its own without treatment. Physiological anemia of the newborn can also be observed in a full-term baby, and the exact cause of this has not been established. This may be due to the destruction of fetal hemoglobin and the low growth rate of hemoglobin type A, as in an adult. This condition also should not cause concern and is transient.

The consequences of anemia in a newborn can be very serious if the pathology was not noticed in time. After all, constant hypoxia leads not only to a lack of body weight, but also a lack of oxygen affects the brain. It is known that iron is necessary for the normal development of the nervous system. Iron deficiency anemia affects neuronal energy metabolism, neurotransmitter metabolism, myelination, and memory function. Therefore, anemia in the neonatal period can cause irreversible memory impairment, delayed psychomotor development, behavioral anomalies, and speech delays in the future. As for other complications, anemia increases the risk of other infectious diseases. The consequence of an untimely diagnosed hemolytic anemia may be brain damage and the development of bilirubin encephalopathy.

stages

Analyzes also allow you to classify anemia by severity:

1. first degree - hemoglobin level within 120 (110) - 91 T / L;
2. the second degree of anemia - 90 - 71 T/L;
3. third degree - hemoglobin level 70-51 T/L;
4. fourth degree - hemoglobin level less than 50 T/L.

Anemia of the 1st degree in a newborn is considered mild and may be a sign of physiological processes, but it must be monitored and monitored. Anemia of a mild degree in a newborn premature baby can also be regarded as transient and requires observation.

Diagnosis of anemia in a newborn

The main criterion for anemia is certainly laboratory confirmation of a decrease in the level of hemoglobin and red blood cells. But the main task of the mother and the doctor is the timely diagnosis of anemia, so it should begin with general clinical signs. The pallor of the skin and mucous membranes should already suggest a possible anemia. If the child is not gaining weight well, then you also need to look for the cause and think about anemia. It is important to ask the mother about pregnancy and childbirth, whether she took vitamins and whether there was massive blood loss. All of these thoughts may lead to a diagnosis. Even if the baby is premature, he, in most cases, has a latent iron deficiency and this is potentially dangerous for the development of anemia in the future.

On examination, in addition to pallor, there may be a systolic murmur at the apex of the heart during auscultation, which also requires attention. This is due to the turbulence of the blood flow at a low concentration of red blood cells relative to the liquid part of the blood. There are practically no other objective symptoms.

Laboratory diagnosis of anemia is the most accurate and necessary for an accurate diagnosis. A general blood test allows you to establish a decrease in the level of red blood cells and hemoglobin. And such a diagnostic number is:

1. decrease in hemoglobin level below 145 T/L in children during the first two weeks of life;
2. hemoglobin level less than 120 T/L in newborns after the second week of life;
3. in children under five years old, less than 110 T / L;
4. in children after five years - less than 120 T / L.

In a general blood test, if anemia is suspected, it is also necessary to determine the level of reticulocytes. These cells are responsible for the formation of red blood cells in the red bone marrow and are their precursors. The level of reticulocytes in the future is necessary to assess the response to treatment.

To establish the diagnosis of iron deficiency anemia, one or more tests should be added to the determination of hemoglobin concentration. Three parameters that provide summary information on iron status are ferritin, chromium, and transferrin concentrations. Ferritin concentration is a sensitive indicator for assessing iron stores in healthy individuals. Measurement of ferritin concentration is widely used in clinical practice and is available abroad. But in Ukraine, of these indicators, only the level of transferrin is used.

To date, most blood tests are carried out on special analyzers that allow, in addition to the formula, to evaluate the size of red blood cells and their structure. In anemia, the mean erythrocyte hemoglobin content is reduced, the mean erythrocyte size is reduced, and the mean erythrocyte hemoglobin concentration is also below normal.

Among other tests, a microscopic examination of the smear is also carried out, which, with anemia, has characteristic changes in the form of anisocytosis, inclusions and granules in red blood cells.

If a child has jaundice combined with anemia, then a study of total bilirubin and its value by fractions is mandatory. It is also necessary to exclude hemolytic anemia or differentiate from hemolytic disease of the newborn. The level of total bilirubin should be in the range of 8.5 - 20.5 micromoles.

These are the main laboratory indicators that can confirm the diagnosis of anemia and establish the etiology.

Instrumental diagnostics for iron deficiency anemia is not used, but if hereditary hemolytic anemia is suspected, an ultrasound examination is possible. It shows the condition of the spleen, which affects the condition of the child with this pathology and indicates treatment options.

Differential Diagnosis

Differential diagnosis of anemia should be carried out primarily according to the etiological principle. It is necessary to distinguish between the symptoms of anemia in a child with physiological jaundice and manifestations of hemolytic anemia. In the first case, a decrease in the level of hemoglobin will be accompanied by an increase in bilirubin below critical values ​​- this is below 100 micromoles. If we are talking about congenital hemolytic anemia, then bilirubin will be above 100, even up to 250 and above. There will also be blood hyperchromia (an increase in the color index above 1.05).

Treatment of anemia in a newborn

Of course, the approach to the treatment of anemia of different etiologies is different. That is why it is so important to know the cause of a particular type of pathology. If we are talking about iron deficiency anemia, which arose after prolonged bleeding in a child or due to congenital pathology of iron absorption, then the first step to treatment is to exclude the cause of anemia.

Speaking of iron deficiency anemia, as the most common problem, it should be noted that the main element in the treatment of such anemia is the replenishment of iron stores. Therefore, the medications that are used in the treatment are iron preparations. Iron is most readily absorbed from the trivalent form, so iron preparations, especially for newborns, should be in this form. Preparations based on ferric iron are better absorbed, better absorbed and have fewer negative and side effects.

Treatment of anemia begins not with the calculation of the drug, but with the calculation of the dose of iron that the child needs. After all, each drug contains a certain amount of iron, which must also be considered when choosing this drug. The therapeutic dose of iron is 3-5 milligrams per kilogram of a child's body weight, which must be taken per day. The minimum treatment period for anemia is one month. Further, if the blood counts are within the normal range, then they give a prophylactic dose for another six months. The prophylactic dose is half of the therapeutic dose, and it is given ten days each month for six months. Medicines that are used to treat iron deficiency anemia are as follows:

1. Aktiferin- This is an iron preparation, which also includes the amino acid serine, which ensures its better absorption. The drug acts when it enters the intestines and bloodstream by binding to the protein transferrin. So iron is transported to the liver, bone marrow, where it is released and takes part in the synthesis of hemoglobin and in the formation of new red blood cells. The drug is available in the form of drops, syrup and capsules. For newborns use the form of drops. One milliliter of the drug in this form contains 9.8 milligrams of iron, which corresponds to 20 drops. Therefore, the dosage is calculated first 3-5 milligrams per child's weight, and then the drug itself. Side effects can be in babies in the form of colic, increased gas formation, diarrhea or constipation. These are the first signs that indicate the need to reduce the dose of the drug. Precautions - do not use the drug for hemolytic anemia.
2. Hemoferon- it is also an iron preparation, which additionally contains other vitamins - folic acid and cyanocobalamin. The composition of the drug includes citric acid, which helps to better absorb the iron molecule. One milliliter of the drug contains 8.2 milligrams of iron. The dosage of the drug is standard, but for newborns, on average, it is 2.5 milliliters daily dose. Side effects can be in the form of vomiting, indigestion and stool, staining of feces in a dark color. Precautions - do not use the drug in case of liver damage in a child or if hepatitis is suspected.
3. Hemopher- This is a drug that contains an iron molecule, divalent and citric acid. It is most suitable for treatments that require rapid hemoglobin results, followed by a switch to trivalent drugs. Dosage of the drug - 1 drop contains 1.6 milligrams of iron, and for newborns about 1 drop per kilogram of body weight. Side effects - loss of appetite and refusal of the breast, diarrhea.
4. Ferramin-Vita- This is a ferric iron preparation, which acts on the principle of slow recovery of iron levels in the child's body. The drug is available in the form of a solution and its dosage is one drop per day for newborns. Side effects are less common than with ferrous iron and may be limited to dyspepsia.
5. Maltofer- This is a preparation of ferric iron, which has a slow absorption in the intestine, and due to this, its physiological concentration in the blood serum is established. The dosage of the drug is 1 drop per kilogram for newborns. The drug in the form of drops can be used by newborns, including premature babies. Side effects can be in the form of allergic manifestations and staining of the stool.

Such treatment of anemia with iron preparations is carried out for a month, then preventive therapy is given. It is very important during this period if the mother is breastfeeding, then her diet should contain the maximum amount of iron and all useful trace elements. If the child is bottle-fed, then it is necessary that the mixture is also enriched with iron. It should be said that in the presence of anemia, the cause of which is a violation of iron absorption, it is necessary to use its injectable forms. The same applies to those cases when the child had an operation on the stomach or intestines and oral forms of iron cannot be used.

It is necessary to evaluate the effectiveness of treatment on the 7-10th day after the start, when it is necessary to repeat the blood test. At the same time, an increase in the number of reticulocytes will be evidence of a positive dynamics of treatment. An increase in hemoglobin will be observed by the end of the course of treatment in the third or fourth week.

Nursing care for neonatal anemia is very important if the anemia is congenital. If we are talking about hemolytic anemia or congenital aplastic anemia, then it is very important to properly organize the child's daily routine, his nutrition. Considering that complications can be due to the influence of bilirubin on the central nervous system, it is important that the medical staff monitor the child. After all, there may be symptoms that threaten the life of the child, and the mother may simply not notice them due to inexperience. Therefore, the issue of treating congenital anemia in a hospital is so important.

Speaking about the surgical treatment of anemia, it should be noted that severe anemia, in which the hemoglobin level is less than 70, requires a blood transfusion. This is considered an intervention at the level of surgery. Be sure to determine the child's blood type and Rh factor.

Surgical treatment of congenital hemolytic anemia is carried out for children at an older age, closer to five years. It is performed in severe anemia with frequent hemolytic crises. The essence of the operation is to remove the spleen. The spleen is an immunocompetent organ in which the destruction of erythrocytes occurs and in hemolytic anemia it is permanent. Therefore, splenectomy results in fewer flare-ups because fewer red blood cells are destroyed. But before such an operation, the child must be vaccinated outside the plan, since such an operation disrupts the normal immune status.

Vitamins for a child with anemia are considered mandatory, as it increases the absorption of iron and has a good effect on appetite. For newborns, vitamins from the carnitine group can be used, which contribute to weight gain, which is important for anemia. One of these drugs is Steatel.

steatel is a vitamin that contains the metabolically active substance levocarnitine. It promotes the absorption of biologically useful substances and accelerates the metabolism in cells, which especially affects the synthesis of new red blood cells. The drug is available in the form of a syrup. One milliliter of syrup contains 100 milligrams of the substance, and the dosage is 50 milligrams per kilogram. The drug can be used even in premature babies. Side effects can be in the form of stool disorders, colic, convulsive syndrome.

Physiotherapeutic treatment of anemia in the acute period in newborns is not used.

Alternative treatment of anemia

Of course, a newborn cannot take anything other than mother's milk and medicines, because there can be an allergy to any herbs or traditional medicine. Therefore, all folk remedies are aimed at ensuring that a young mother who feeds a child follows the advice of traditional medicine, taking certain means.

1. The main thing for the treatment of anemia is to eat right for the mother in order to improve hematopoiesis for both herself and the child. Therefore, if a newborn has iron deficiency anemia, then the mother should include in her diet the maximum amount of foods that contain iron. These products include: red meat, fish, buckwheat porridge, parsley and spinach, legumes, pomegranate. These foods must be included in the diet.
2. Pomegranate is known for its beneficial effect not only on blood vessels, but also on the heart and on the formation of formed elements. Therefore, to stimulate erythropoiesis, you need to take 150 grams of fresh pomegranate juice, add 50 grams of beet juice and the same amount of carrot juice. You need to take this vitamin mix four times a day. These products are very allergenic, so you need to start with a small amount - ten to twenty grams. You can drink throughout the month.
3. Another folk remedy is the use of blueberry extract. To do this, you need to take two hundred grams of fresh berries and pour 50 grams of water. You need to insist for two hours, and then beat with a blender. Mom needs to take a tablespoon five times a day in the intervals between feedings.

Herbal treatment for anemia is also widely used:

1. Hellebore and yarrow grass should be taken in equal proportions and poured with hot water. This tincture should be allowed to stand for two days, and then you can take a teaspoon in the morning and evening, adding a little lemon juice.
2. Rose hips must be poured with hot water and steeped for ten to twenty minutes. Mom should take a glass throughout the day instead of tea. Such tea not only accelerates the synthesis of red blood cells, but also accelerates the work of the liver, which synthesizes proteins, including transferrin. Such a complex action brings recovery closer.
3. Birch leaves must be dried in the oven and made into a decoction. To do this, take thirty grams of dry leaves and pour a liter of hot water. After insisting, after two hours, you can take a decoction of a tablespoon twice a day.

Homeopathic remedies can also be used in mom:

1. Natrum chloratum is a homeopathic medicine based on organic elements. It is produced as a monopreparation in granules or in combination with succinic acid, which has a better effect on iron absorption. The dosage of the drug for the mother depends on the severity of anemia - in the first degree, two granules three times, and in more severe cases, the dose is doubled. There may be side effects in the form of pallor of the skin and mucous membranes of the child, which is caused by the action of the drug and will disappear after a few days.
2. Poetam is a multicomponent drug, which mainly consists of different types of antibodies to erythropoietin in homeopathic concentrations. The effect of the drug is to stimulate the work of cells that are precursors of red blood cells. The dosage of the drug is 1 tablet per day or six drops once a day. Side effects - an increase in body temperature to subfebrile figures.
3. Cuprum metalicum is a homeopathic remedy that contains copper molecules that accelerate the maturation of red blood cells in the red bone marrow. The drug is used for mom at a dose of one grain six times a day. Side effects can only be with intolerance by the mother, and the newborn may have problems with stool.
4. Galium-Hel is a combined remedy in homeopathy, which is used to treat anemia, which is accompanied by weight loss in the child, poor appetite, and stool disorders in the form of diarrhea. The drug is dosed five drops three times a day for the mother, since the child is not recommended in the acute period. The first three days you can take five drops every three hours. Side effects were not found.

Prevention

Prevention of anemia must be carried out by the mother during pregnancy. You need to start with the correct regimen of the mother's day and nutrition, as well as taking vitamins containing iron. But for a newborn, prevention should be taking iron supplements for premature babies and babies at risk. All premature babies should consume iron at a dose of at least 2 mg/kg per day up to and including 12 months of age (this is the amount of iron obtained from iron-fortified formula milk). Premature infants who are breastfed should receive iron supplements at a dose of 2 mg/kg per day no later than 1 month of age and until the child is switched to feeding iron-fortified formula or begins to receive complementary foods, which will ensure the intake of iron at a dose of 2 mg / kg. An exception should be made for infants who have received iron loads from multiple red blood cell transfusions.

Forecast

The prognosis of anemia is favorable with proper and timely treatment, when it comes to iron deficiency. Congenital aplastic anemias have a poor prognosis, children usually live five to six years. Congenital hemolytic anemia has a good prognosis for life, if all crises are correctly corrected and comorbidities are treated.

Anemia in newborns is very common, especially if the mother had certain problems during pregnancy or childbirth. Most often, one has to deal with iron deficiency anemia, which, with the right treatment tactics, are well corrected. But if the family has congenital anemia, then you need to consult a doctor even during pregnancy planning.

Hemolytic disease of the newborn (HDN): causes, manifestations, how to treat

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

What is hemolytic disease of the newborn?

TTH is the result 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 to the antigens on the surface of the erythrocytes of the fetus (first of all, this is). Simply put, they contain proteins that are recognized by the mother's body as foreign. That is why in the body of a pregnant woman, the processes of activation of her immune system begin. What is going on? So, in response to the ingestion of an unfamiliar protein, biosynthesis of specific molecules occurs that can bind to 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 TTH, 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 present level of development of medicine, there are at least 100 different systems of antigenic proteins present on the erythrocyte membrane. The following are the most well studied:, Rhesus, Kell, Duffy. But, unfortunately, the erroneous judgment is very common 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 at all that incompatibility is ruled out for this antigen in a pregnant woman. This is the exposure 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 type, Rh factor and Rh conflict

The likelihood of conflict if the mother is Rh-negative, and the father is Rh-positive

Very often, a woman who has a negative Rh worries about her future offspring, even before she is pregnant. She is afraid of the possibility of developing a Rhesus conflict. Some are even afraid to marry a Rh-positive man.

But is it justified? And what is the probability of developing an immunological conflict in such a pair?

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

• The allele of one gene contains a dominant trait, which is the leading one and manifests itself in the body (in our case, the Rh factor is positive, we will 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, we will denote it with a small letter r).

What does this information give us?

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

In this case, the mother, who is Rh-negative, contains only two recessive traits (rr). As you know, during inheritance, each parent can give his child only one trait.

Table 1. Probability of inheriting 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)

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

So, we can draw a simple and obvious conclusion: the judgment that immunological incompatibility must certainly be in a Rh-negative mother and a Rh-positive father 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 affiliation, this does not mean at all that the development of HDN is inevitable. Do not forget about the protective properties. With a physiologically proceeding pregnancy, the placenta practically does not pass antibodies from mother to child. The proof is the fact that hemolytic disease occurs only in the fetus of every 20th Rh-negative woman.

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

Upon learning about the belonging of their blood, women with a similar combination of group and Rhesus 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 HDN. However, the usual 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. So laid down by nature, these antibodies are called alpha and beta agglutinins, they are present in all representatives of the first group. And when a small amount of fetal erythrocytes enter the mother's bloodstream, they are destroyed by the already existing agglutinins. Thus, antibodies to the Rh factor system simply do not have time to form, because agglutinins are ahead of them.

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

Which women are at risk?

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

1. Lifetime blood transfusion in an Rh-negative woman

This is especially true for those who have had various allergic reactions after transfusion. Often in the literature one can find a judgment that it is precisely those women who are transfused with a blood group without taking into account the Rh factor that are at risk. But is it possible in our time? Such a probability is practically excluded, since the Rh affiliation is checked at several stages:

• When taking blood from a donor;
• at the transfusion station;
• The laboratory of the hospital where blood transfusion is carried out;
• A transfusiologist who conducts a three-fold test of the compatibility of the blood of the donor and the recipient (the person who is to be transfused).

The question arises: how then can a woman be 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" in whose blood there are 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 in the recipient's body, specific antibodies can begin to be produced in a small amount, but even their amount is enough for the immune system to “remember” this antigen. Therefore, in women with a similar situation, even in the case of the first pregnancy, an immune conflict may arise between the body of her and the child.

2. Re-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 proceed with the formation of antibodies and immunological incompatibility. And indeed it is. But many people forget that the first pregnancy should be considered the fact of the development of the fetal egg in the mother's body before any period.

Therefore, at risk are women who have had:

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

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

• Detachment of the chorion, placenta during this pregnancy;
• Formation of a post-placental hematoma;
• Bleeding with low placenta previa;
• Women who used invasive diagnostic methods (piercing of the fetal bladder with amniotic fluid sampling, blood sampling from the umbilical cord of the fetus, biopsy of the chorion site, 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 between fetal and neonatal hemolytic disease?

There are no fundamental differences between these concepts. Just hemolytic disease in the fetus occurs in the prenatal period. HDN means the course of the pathological process after the birth of the child. In this way, the difference lies only in the conditions of the baby's stay: in utero or after childbirth.

But there is another difference in the mechanism of the course of this pathology: during pregnancy, the mother's antibodies continue to enter the fetus, 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 forbidden to breastfeed their baby. This is necessary in order to exclude the entry of antibodies into the baby's body and not aggravate the course of the disease.

How is the disease progressing?

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

1. Anemic- the main symptom is a decrease in the 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 the subcutaneous tissue;
• In the chest and abdominal cavity;
• In the pericardial sac;
• In the placenta (during the prenatal period)
• Hemorrhagic rashes on the skin are also possible;
• Sometimes there is a violation of the function of blood clotting;
• The child is pale, lethargic, weak.

3. Icteric form characterized, which is formed as a result of the destruction of red blood cells. With this disease, toxic damage to all organs and tissues occurs:

• The most severe option is the deposition of bilirubin in the liver and brain of the fetus. This condition is called "nuclear jaundice";
• Yellowish staining 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);
• Perhaps the development of diabetes mellitus with damage to the pancreas.

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 percentage of mortality.

How to determine the severity of the disease?

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

Diagnostic methods

Already during pregnancy, you can 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, guided by several research methods.

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

• Enlargement of the placenta;
• The presence of fluid in the tissues: fiber, chest, abdominal cavity, swelling of the soft tissues of the fetal head;
• Increase in the speed of blood flow in the uterine arteries, in the vessels of the brain;
• The presence of suspension in the amniotic fluid;
• Premature aging of the placenta.

3. Increasing the density of amniotic fluid.

4. At registration - signs and violation of the heart rhythm.

5. In rare cases, a cord blood test is performed.(determine the level of hemoglobin and bilirubin). This method is dangerous 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 type, Rh factor.
• Examination of the child (in severe cases, jaundice and swelling are pronounced).
• Determination of antibodies in the blood of a child.

Treatment of HDN

You can start treatment for this disease during pregnancy, to prevent deterioration of the fetus:

1. The introduction of enterosorbents into the mother's body, for example, "Polysorb". This drug helps to reduce the titer of antibodies.
2. Drip administration of glucose and vitamin E solutions. These substances strengthen the cell membranes of red blood cells.
3. Injections of hemostatic drugs: "Dicinon" ("Etamzilat"). They are needed to increase blood clotting ability.
4. In severe cases, an intrauterine fetus may be required. However, this procedure is very dangerous and fraught with adverse consequences: fetal death, premature birth, etc.

Methods for treating a child after childbirth:

With a severe degree of the disease, the following methods of treatment are used:

1. Blood transfusion. It is important to remember that only “fresh” blood is used for blood transfusion, the date of preparation of which does not exceed three days. This procedure is dangerous, but it can save the baby's life.
2. Purification of blood with the help of hemodialysis and plasmapheresis devices. These methods contribute to the removal of toxic substances from the blood (bilirubin, antibodies, erythrocyte destruction products).

Prevention of the development of immune conflict during pregnancy

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

• Try not to have abortions, for this you need to consult a gynecologist for the appointment of reliable methods of contraception.
• Even if the first pregnancy went well, without complications, then after childbirth, within 72 hours, it is necessary to introduce 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, one 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, due attention must be paid to prevention issues in order to avoid potential problems as much as possible.