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The occurrence of an immune conflict underlying hemolytic disease of the newborn is possible if the mother is antigen-negative and the fetus is antigen-positive. With the development of HDPiN according to the Rh factor, the mother's red blood cells are Rh negative, and the fetus's red blood cells are Rh positive, i.e. contain O-factor. The realization of the conflict (development of HDPiN) usually occurs during repeated pregnancies, since previous sensitization is necessary.

Hemolytic disease of newborns due to group incompatibility develops with 0(1) blood group in the mother and A(II) or, less commonly, B(III) blood group in the fetus. The realization of the conflict is possible already during the first pregnancy. HBPiN can also occur due to incompatibility with other rare antigen systems: Kell, Lutheran, etc.

How does hemolytic disease of the newborn develop?

For the development of hemolytic disease of the newborn, it is necessary for antigen-positive erythrocytes of the fetus to enter the bloodstream of an antigen-negative pregnant woman. In this case, it is not so much the fact of transplacental transfer of fetal red blood cells that is of great importance, but the amount of fetal blood entering the mother’s body. Factors contributing to isoimmunization, especially for the Rh factor, include:

• previous medical and non-medical abortions;
• previous spontaneous (one or more) miscarriages;
• previous ectopic pregnancy;
• previous births (premature and term);
• invasive diagnostic methods (amniocentesis, cordocentesis, chorionic villus biopsy);
• threat of miscarriage.

The disease is based on hemolysis (destruction) of red blood cells, caused by the incompatibility of the blood of the mother and fetus according to the Rh factor, group and other blood factors, which occurs in the 3-4th month of intrauterine development and sharply increases after birth.

When antigen-positive red blood cells of the fetus enter the bloodstream of an antigen-negative woman, anti-Rhesus or group antibodies are produced in her body. If the antibodies belong to the IgG class, they pass transplacentally into the fetal bloodstream and bind to antigen-positive fetal red blood cells, causing their hemolysis.

The Rh antigen system consists of six main antigens: C, c, D, d, E and e. Rh-positive red blood cells contain the D factor, and Rh-negative red blood cells do not contain it, although other Rh antigens are often found in them. During the first pregnancy, fetal erythrocytes that have a D antigen that have entered the bloodstream of an Rh-negative pregnant woman initially lead to the synthesis of Rh antibodies, which are class M immunoglobulins, which do not penetrate the placenta. Class G immunoglobulins are then produced, which are able to cross the placental barrier. Due to the small number of fetal red blood cells and immunosuppressive mechanisms, the primary immune response in the pregnant woman is reduced. That is why conflict with Rh incompatibility practically does not occur during the first pregnancy, and the child is born healthy. With repeated pregnancies, the development of a conflict is possible, and the child is born with hemolytic disease of the newborn.

A and B antigens are located on the outer surface of the plasma membrane of the red blood cell. Isoimmune anti-A and anti-B group antibodies belong to the IgG class, in contrast to natural group antibodies - calamus, which belong to the IgM class. Isoimmune antibodies can combine with the corresponding antigens A and B and become fixed to other tissues, including the tissues of the placenta. This is why hemolytic disease of the newborn according to the ABO system can develop already during the first pregnancy, but only in about 10% of cases.

When it is possible to implement both variants of the conflict, a conflict occurs more often in the AB(0) system.

But not only the Rh factor is the cause of the development of the disease. It can occur due to blood incompatibility and other factors. In addition, hemolytic disease of the fetus can occur when the blood of the mother and fetus do not match the main blood groups of the ABO system. Antigens A and B, inherited from the father, can cause the formation of incomplete agglutinins in a mother with blood type 0, which, unlike ordinary α- and β-agglutinins, can pass through the placental barrier and cause hemolysis of fetal red blood cells. Conflict based on inconsistency according to the AB0 system occurs in 10% of cases and, as a rule, proceeds benignly. It should be noted that a mismatch between the blood of the fetus and mother does not always lead to the development of the disease. For example, Rh incompatibility occurs in 5-10% of pregnancies, and Rh conflict - in 0.8%.

Pathogenesis in the edematous form of hemolytic disease of the newborn

The edematous form, or fetal hydrops, occurs if hemolysis begins in utero, from approximately 18-22 weeks of pregnancy, is intense and leads to the development of severe fetal anemia. As a result, severe fetal hypoxia occurs, which causes profound metabolic disorders and damage to the vascular wall. Increased permeability of the vascular wall leads to the fact that albumin and water move from the fetal blood into the tissue interstitium. At the same time, the synthesis of albumin in the baby’s liver decreases, which aggravates hypoproteinemia.

As a result, a general edema syndrome is formed in utero, ascites develops, fluid accumulates in the pleural cavities, in the pericardial cavity, etc. A decrease in the drainage function of the lymphatic system aggravates the development of ascites and the accumulation of fluid in other cavities of the body. Hypoproteinemia, accumulation of fluid in the cavities in combination with damage to the vascular wall lead to the development of heart failure.

As a result of erythroid metaplasia in organs and severe fibrosis in the liver, hepato- and splenomegaly is formed. Ascites and hepatosplenomegaly cause a high position of the diaphragm, which leads to pulmonary hypoplasia. The increased amount of indirect bilirubin formed during hemolysis is removed from the blood and tissues of the fetus through the placenta into the mother’s body, so there is no jaundice at birth.

Pathogenesis in the icteric form of hemolytic disease of the newborn

The icteric form of the disease develops if hemolysis begins shortly before birth. As a result of the destruction of red blood cells, the concentration of indirect (unconjugated) bilirubin quickly and significantly increases, which leads to the following changes:

• the accumulation of indirect bilirubin in the lipid substances of tissues, which causes icteric staining of the skin and sclera - jaundice, as well as as a result of the accumulation of indirect bilirubin in the nuclei of the base of the brain, which leads to its damage with the development of neuronal necrosis, gliosis and the formation of bilirubin encephalopathy (kernicterus);
• increased load on liver glucuronyltransferase, which leads to depletion of this enzyme, the synthesis of which begins in liver cells only after birth, and as a result hyperbilirubinemia is maintained and intensified;
• increased excretion of conjugated (direct) bilirubin, which can lead to impaired bile excretion and the development of a complication - cholestasis.

As with the edematous form, hepatosplenomegaly develops.

Pathogenesis of the anemic form of hemolytic disease

The anemic form develops when small amounts of maternal antibodies enter the fetal bloodstream shortly before birth. At the same time, hemolysis is not intense, and the newborn’s liver quite actively removes indirect bilirubin. Anemia dominates, and jaundice is absent or minimally expressed. Hepatosplenomegaly is characteristic.

Symptoms of hemolytic disease of newborns

Hemolytic disease of the newborn and fetus has three clinical forms: anemic, icteric and edematous. Among them, the most severe and prognostically unfavorable is edematous.

General clinical signs of all forms of hemolytic disease of the newborn: pallor of the skin and visible mucous membranes as a result of anemia, hepatosplenomegaly. Along with this, edematous, icteric and anemic forms have their own characteristics.

Edema form

The most severe form of hemolytic disease of the newborn. The clinical picture, in addition to the above symptoms, is characterized by a common edematous syndrome: anasarca, ascites, hydropericardium, etc. The appearance of hemorrhages on the skin, the development of disseminated intravascular coagulation syndrome as a consequence of hypoxia, and hemodynamic disturbances with cardiopulmonary failure are possible. The expansion of the boundaries of the heart and the mutedness of its tones are noted. Often after birth, respiratory disorders develop against the background of pulmonary hypoplasia.

Jaundice form of hemolytic disease

This is the most common form of hemolytic disease of the newborn. In addition to general clinical manifestations, which include pallor of the skin and visible mucous membranes, as a rule, very moderate and moderate enlargement of the spleen and liver, jaundice of a predominantly warm yellow hue is also noted. At the birth of a child, amniotic fluid, umbilical cord membranes, and vernix may be stained.

The early development of jaundice is characteristic: it occurs either at birth or in the first 24-36 hours of a newborn’s life.

According to the severity of jaundice, there are three degrees of the icteric form of hemolytic disease of the newborn:

• mild: jaundice appears at the end of the first or at the beginning of the second day of the child’s life, the bilirubin content in the umbilical cord blood does not exceed 51 µmol/l, the hourly increase in bilirubin is up to 4-5 µmol/l, moderate enlargement of the liver and spleen is less than 2.5 and 1.0 cm respectively;
• moderate: jaundice occurs immediately at birth or in the first hours after birth, the amount of bilirubin in the umbilical cord blood exceeds 68 µmol/l, the hourly increase in bilirubin is up to 6-10 µmol/l, liver enlargement is up to 2.5-3.0 cm and spleen up to 1.0-1.5 cm;
• severe: diagnosed according to ultrasound of the placenta, optical density of amniotic fluid bilirubin obtained during amniocentesis, the amount of hemoglobin and blood hematocrit value obtained during cordocentesis. If treatment is not started in a timely manner or is inadequate, the icteric form may be accompanied by the development of the following complications.

Kernicterus

In this case, symptoms indicating damage to the nervous system are noted. First, in the form of bilirubin intoxication (lethargy, pathological yawning, loss of appetite, regurgitation, muscle hypotonia, disappearance of phase II of the Moro reflex), and then bilirubin encephalopathy (forced body position with opisthotonus, “brain” cry, bulging of the large fontanel, disappearance of the Moro reflex , convulsions, pathological oculomotor symptoms - the “setting sun” symptom, nystagmus, etc.).

Bile thickening syndrome, when jaundice acquires a greenish tint, the liver is slightly enlarged compared to previous days, a tendency to acholia appears, and the color of urine increases in saturation.

Anemic form of hemolytic disease of the newborn

The least common and mildest form of the disease. Against the background of pallor of the skin, lethargy, poor sucking, tachycardia, hepatosplenomegaly are noted, and possible muffled heart sounds and systolic murmur.

Along with changes in the fetus’s body, there are changes in the placenta. This is expressed in an increase in its mass. If normally the ratio of placenta weight to fetal weight is 1:6, then with Rh conflict it is 1:3. Enlargement of the placenta occurs mainly due to its edema.

But the pathology of Rhesus conflict is not limited to this. In addition to the above, with Rh conflict, antenatal (prenatal) fetal death and repeated spontaneous abortions are observed.

Moreover, with high antibody activity, spontaneous abortions can occur in the early stages of pregnancy.

Women who have had a Rhesus conflict are more likely to develop toxicosis of pregnancy, anemia, and impaired liver function.

Classification

Depending on the type of conflict, hemolytic disease of newborns is distinguished:

• in case of incompatibility of red blood cells of mother and fetus according to the Rh factor;
• in case of incompatibility according to the ABO system (group incompatibility);
• in case of incompatibility for rare blood factors.

According to clinical manifestations there are:

• edematous form (anemia with dropsy);
• icteric form (anemia with jaundice);
• anemic form (anemia without jaundice and dropsy).

According to the severity, the icteric form is classified as mild, moderate and severe.

In addition, there are complicated (kernicterus, bile thickening syndrome, hemorrhagic syndrome, damage to the kidneys, adrenal glands, etc.) and uncomplicated forms of hemolytic disease of the newborn.

Diagnosis of hemolytic disease of newborns

Diagnosis of hemolytic disease of newborns is based on an immunological examination of the pregnant woman, ultrasound, Doppler measurements of fetal-placental and uteroplacental blood flow, electrophysiological examination methods, examination of amniotic fluid (during amniocentesis), cordocentesis and fetal blood testing.

An immunological study allows you to determine the presence of antibodies, as well as changes in their quantity (increase or decrease in titer). Ultrasound allows you to measure the volume of the placenta, determine an increase in its thickness, detect polyhydramnios, an increase in the size of the fetal liver and spleen, an increase in the size of the fetal abdomen compared to the size of the head and chest, and ascites in the fetus. Doppler measurements can detect an increase in the systolic-diastolic ratio and resistance index in the umbilical cord artery and an increase in blood flow velocity in the middle cerebral artery of the fetus. Electrophysiological methods (cardiotocography with determination of the fetal condition indicator) make it possible to detect a monotonous rhythm in moderate and severe forms of the disease and a “sinusoidal” rhythm in the edematous form of HDP. The study of amniotic fluid (during amniocentesis) allows us to determine the increase in the optical density of bilirubin in the amniotic fluid. Finally, cordocentesis and fetal blood testing can detect a decrease in hematocrit, a decrease in hemoglobin, an increase in bilirubin concentration, conduct an indirect Coombs test and determine the fetal blood type and the presence of the Rh factor.

Since the prognosis for the disease depends on the content of bilirubin, in order to develop further medical tactics in a child born with suspected hemolytic disease of the newborn, it is first necessary to do a biochemical blood test to determine the concentration of bilirubin (total, indirect, direct), protein, albumin, AST, ALT, and then conduct an examination to determine the etiology of hyperbilirubinemia. For this purpose, the newborn is given a general blood test, the Rh-type is determined for possible Rh-sensitization and the blood group for possible ABO-sensitization, the antibody titer is determined and the direct Coombs test is performed.

Differential diagnosis

Differential diagnosis of hemolytic disease of newborns is carried out with other anemias. These include hereditary anemia caused by the following disorders:

• disturbance of erythrocyte morphology (microspherocytosis, elliptocytosis, stomatocytosis);
• deficiency of erythrocyte enzymes (glucose-6-phosphate dehydrogenase, glutathione reductase, glutathione peroxidase, pyruvate kinase);
• anomaly of hemoglobin synthesis (a-thalassemia).

To exclude these diseases, you should carefully collect anamnesis about the presence of other carriers of this pathology in the family and conduct the following studies:

• determination of erythrocyte morphology;
• determination of osmotic resistance and diameter of red blood cells;
• determination of erythrocyte enzyme activity;
• determination of hemoglobin type.

Treatment of hemolytic disease of newborns

First of all, if we are talking about Rh conflict, it is necessary to diagnose the disease during the period of intrauterine development of the fetus, assess its severity and, accordingly, the prognosis of the disease, and carry out treatment until the fetus reaches viability. All treatment and prophylactic methods used during this period of fetal life are divided into non-invasive and invasive.

Non-invasive methods

Non-invasive methods include plasmapheresis and administration of intravenous immunoglobulin to the pregnant woman.

Plasmapheresis of a pregnant woman is carried out for the purpose of detoxification, rheocorrection and immunocorrection.

Contraindications to plasmapheresis:

• severe damage to the cardiovascular system;
• anemia (hemoglobin less than 100 g/l);
• hypoproteinemia (less than 55 g/l);
• hypocoagulation;
• immunodeficiency state;
• history of allergic reactions to protein and colloid drugs, anticoagulants.

Immunoglobulin for intravenous administration is used to inhibit the production of one's own maternal antibodies and blockade of Rh-bound antibodies during their placental transport. Immunoglobulin is used for intravenous administration at a dose of 0.4 g per kilogram of the pregnant woman’s body weight. This dose is distributed over 4-5 days. Courses of administration must be repeated every 3 weeks until delivery. This method of treatment is not considered generally accepted, since in severe cases the outcome for the fetus improves only slightly.

Invasive methods

Invasive methods include cordocentesis and intrauterine red blood cell transfusion. These procedures are carried out only for Rh sensitization; currently this is the only pathogenetic method of treating hemolytic disease of the fetus.

Indications for cordocentesis:

• burdened obstetric history (death of previous children from severe forms of hemolytic disease of the newborn);
• high antibody titer (1:32 and above);
• Ultrasound shows signs of hemolytic disease of the fetus;
• high values ​​of the optical density of bilirubin in amniotic fluid obtained during amniocentesis (zone 3 of the Lily scale).

Timing during which cordocentesis is performed: from the 24th to the 35th week of pregnancy.

The indication for intrauterine transfusion of red blood cells when a positive Rh factor is detected in the fetus is a decrease in hemoglobin and hematocrit by more than 15% of the norm determined at a given stage of pregnancy. For intrauterine transfusion of red blood cells, only “washed” red blood cells of blood group 0(1) Rh-negative are used. Intrauterine transfusion of red blood cells is carried out according to indications 1-3 times.

Treatment of hemolytic disease of the newborn, in contrast to the treatment of hemolytic disease of the fetus, includes, first of all, the treatment of hyperbilirubinemia, secondly, the correction of anemia and, finally, syndromic therapy aimed at restoring the functions of various organs and systems. All newborns with this disease are not put to the breast, but are fed artificially in the first 5-7 days of life, since antibodies can pass through a woman’s breast milk and be absorbed in the intestines of newborns, which leads to increased hemolysis.

Treatment of hyperbilirubinemia

Treatment of hyperbilirubinemia involves the use of conservative and surgical therapy. They begin with conservative treatment, and if bilirubin levels are critical, they are combined with surgical replacement (exchange) blood transfusion (BCT).

Conservative therapy includes phototherapy (PT) and the use of intravenous immunoglobulin. Infusion therapy, according to the recommendation of the Russian Association of Perinatal Medicine Specialists (RASPM), is carried out in cases where it is impossible to adequately feed the child. Phenobarbital is currently practically not used due to the fact that the onset of the effect is significantly delayed from the start of its use and the use causes an increase in the syndrome of central nervous system depression.

Phototherapy

The mechanism of action of phototherapy is based on the fact that when it is carried out on irradiated areas in the skin and subcutaneous fat layer at a depth of 2-3 mm, as a result of the processes of photooxidation and photoisomerization, a water-soluble isomer of indirect bilirubin is formed - lumirubin, which then enters the bloodstream and is excreted in the bile and urine.

Indications for phototherapy:

• yellowness of the skin at birth;
• high concentration of indirect bilirubin.

Principles of phototherapy:

• radiation dose - not less than 8 μW/(cm2xnm);
• the distance from the source to the patient specified in the instructions for the device should be observed;
• the child should be placed in an incubator;
• the child’s eyes and genitals should be protected;
• The child’s position under the PT lamps should be changed every 6 hours.

Minimum values ​​of indirect bilirubin concentration (µmol/l), at which phototherapy is indicated

Phototherapy is carried out continuously with breaks for feeding the child for 3-5 days. PT should be discontinued when the level of indirect bilirubin decreases below 170 µmol/l.

Various reactions and side effects may occur during phototherapy.

Complications and side effects of phototherapy

If signs of cholestasis appear, as evidenced by an increase in the direct bilirubin fraction by 20-30% or more, an increase in the activity of AST and ALT, alkaline phosphatase, cholesterol concentration, the time of phototherapy should be limited to 6-12 hours/day or completely canceled to avoid development "bronze child" syndrome.

Use of immunoglobulin

Immunoglobulin for intravenous administration is used to block Fc receptors, which prevents hemolysis. Early initiation of immunoglobulin administration is necessary (in the first 2 hours of life), which is only possible with antenatal diagnosis of the disease. Later administration of immunoglobulin is possible, but less effective.

Standard immunoglobulins for intravenous administration are used: sandoglobin, ISIVEN (Italy), polyglobin Np (Germany), etc.

Possible regimens for administering immunoglobulins:

• 1 g/kg every 4 hours;
• 500 mg/kg every 2 hours;
• 800 mg/kg daily for 3 days.

Regardless of the dose and frequency, a proven (95%) positive effect was obtained, which was manifested in a significant reduction in the frequency of PCD and the duration of phototherapy.

Infusion therapy

Infusion therapy is carried out in cases where it is not possible to adequately feed the child during phototherapy. The daily volume of fluid administered to the child must be increased by 10-20% (in children with extremely low body weight - by 40%) compared to the physiological need.

When conducting infusion therapy, you should monitor the child’s body weight, evaluate diuresis, electrolyte levels, blood glucose, and hematocrit.

Infusion therapy primarily involves transfusion of a 10% glucose solution4. Infusion therapy is carried out intravenously or intragastrically through a gastric tube. Intragastric fluid administration can begin from the 3-4th day of life; to prevent the development of cholestasis, a 25% solution of magnesium sulfate at the rate of 5 ml/kg, no-spa - 0.5 ml/kg, 4% potassium solution can be added to the dropper chloride - 5 ml/kg. With intragastric fluid administration, there is no need to reduce the volume of feedings.

Surgical therapy - replacement blood transfusion

There are early (in the first 2 days of life) and late (from the 3rd day of life) PCD.

The indication for late PCD is the concentration of indirect bilirubin equal to 308-340 µmol/l (for a full-term newborn).

Indications for late exchange blood transfusion in newborns depending on body weight at birth

1 * Minimum bilirubin values ​​are an indication for the initiation of appropriate treatment in cases where the child’s body is affected by pathological factors that increase the risk of bilirubin encephalopathy (anemia; Apgar score at 5 minutes less than 4 points; Pa02 less than 40 mm Hg. lasting more than 1 hour; arterial blood pH less than 7.15 lasting more than 1 hour; rectal temperature less than 35 ° C; albumin concentration less than 25 g/l; deterioration of neurological status due to hyperbilirubinemia; generalized infectious disease or meningitis).

When the first symptoms of bilirubin intoxication appear, immediate POC is indicated, regardless of the concentration of bilirubin.

Selection of drugs for replacement blood transfusion

In case of isolated Rh conflict, Rh-negative red blood cells and plasma of the same group as the child’s blood are used, but it is possible to use AB(IV) blood group plasma. In case of an isolated group conflict, red blood cell mass of group 0(1), which matches the Rh factor of the child’s red blood cells, and plasma AB(IV) or one group with the child’s blood group are used. If it is possible to develop both Rh-incompatibility and ABO incompatibility, as well as after intrauterine blood transfusions, Rh-negative red blood cells of the 0(1) blood group and plasma AB(IV) or the same group as the child’s blood group are used for PCD.

In case of hemolytic disease of a newborn with a conflict regarding rare blood factors, donor blood that does not have a “conflict” factor is used.

Calculation of the volume of drugs for exchange blood transfusion

The total volume is 1.5-2 bcc, i.e. for a full-term baby, about 150 ml/kg, and for a premature baby, about 180 ml/kg.

The ratio of red blood cells to plasma depends on the initial hemoglobin concentration before surgery. The total volume consists of the volume of red blood cells required to correct anemia, and the volume of red blood cells and plasma required to achieve the volume of the PCC. The volume of red blood cells required to correct anemia is calculated using the formula:

volume of erythrocyte mass (ml) = (160 - child’s hemoglobin in g/l) x 0.4 x child’s weight in kg.

The volume of red blood cells required to correct anemia should be subtracted from the total volume; the remaining volume is replenished with red blood cells and plasma in a ratio of 2:1. The above approximately corresponds to the following ratio of red blood cell mass depending on the hemoglobin concentration in the child.], , ,

Exchange transfusion technique

The PCA is carried out through one of the large vessels (umbilical vein, subclavian vein). Before POC, blood is drawn to determine the concentration of bilirubin and the compatibility of the blood of the donor and recipient. ZPK is carried out using the “pendulum method”, i.e. removing and introducing alternately a portion of blood at the rate of up to 5-7 ml per kilogram of the child’s weight. Before the start of PCD, it is possible to administer plasma at a rate of 5 ml/kg. ZPK begins with the removal of blood. Before the start of PCD and throughout it, the catheter is washed with sodium heparin solution.

When the initial hemoglobin concentration is below 80 g/l, PCP begins with the correction of anemia, i.e. with the introduction of only red blood cells under the control of hemoglobin content. After reaching a hemoglobin concentration of 160 g/l, red blood cells and plasma are administered. To do this, you can dilute the red blood cells with plasma, or you can alternately inject two syringes of red blood cells and one syringe of plasma.

At the end of the PCA, blood is taken again to determine the concentration of bilirubin. After PCO, conservative therapy is continued.

PCO may be accompanied by the development of immediate and delayed side effects.

Complications of exchange transfusion

Late anemia develops 2-3 weeks after PCO. Usually it is hyporegenerative and hypoerythropoietic in nature. To correct it, recombinant erythropoietin is used (epoetin alfa subcutaneously 200 IU/kg once every three days for 4-6 weeks).

If iron deficiency is detected during treatment with recombinant erythropoietin, iron supplements are included in the therapy at a dose of 2 mg/kg orally for utilized iron.

Prevention

Prevention is designed for women with Rh-negative blood. There is no prevention for group incompatibility.

To prevent the development of Rh sensitization, all women with Rh-negative blood should be given one dose of anti-Rhesus immunoglobulin.

To prevent all the negative consequences of Rh-conflict and conflict due to other blood factors, it is necessary to determine the blood type of the expectant mother and, if it turns out that there is Rh-negative blood, then you should find out whether this woman has been transfused with Rh-positive blood (and in general, whether any blood was transfused); find out what kind of pregnancy there is (whether there have been artificial or spontaneous abortions, intrauterine fetal death, premature birth or death of a newborn soon after birth from jaundice). Information about the Rh status of the father of the unborn child is also important.

For the purpose of prevention, in addition to everything listed earlier, anti-Rhesus immunoglobulin is used. This is done either after the birth of an Rh-positive child, or after the first artificial abortion. It is administered intramuscularly to the postpartum woman, once, no later than 72 hours after birth. This specific prevention of Rh-conflict is possible only in non-sensitized women (sensitization - increased sensitivity), that is, in those who have not been transfused with Rh-positive blood, they have not had abortions or miscarriages, and, in general, this is the first pregnancy.

In addition to specific prevention, nonspecific prevention is also carried out. It includes various medications that reduce the body’s sensitization and increase its immunobiological defenses. Sometimes, for the same purpose, the pregnant woman uses her husband’s skin graft.

Hemolytic disease of the newborn (HDN) is considered a pathological and rather serious condition that develops as a result of intensive destruction of red blood cells. This problem is the main cause of jaundice that appears after childbirth. It is detected in approximately 0.6% of newborns.

The main causes of this pathological condition

Hemolytic disease of newborns manifests itself against the background of complete or partial blood incompatibility between the organisms of the expectant mother and child. This most often occurs in the following situations:

• in case of Rh conflict, which develops if a woman has a negative Rh factor, and the fetus has a positive one;
• development of an immune conflict if the mother’s blood belongs to the O(I) group, and the child’s blood belongs to A(II) or B(III);

• the birth of a child with this pathology is possible only if the woman has increased sensitivity to blood, which differs in some characteristics from her own. This condition develops in the case of previously suffered spontaneous or artificially induced abortions. In the presence of a negative Rh factor, the expectant mother may be sensitized in the event of a transfusion of Rh-positive blood;
• the likelihood of developing Rh conflict in a child who is the second in line increases significantly. After the birth of the first baby, the woman’s body becomes familiar with foreign particles in the blood, which leads to sensitization;
• with the development of this pathological condition against the background of blood group incompatibility, the number of previous pregnancies does not play a big role. Throughout life, sensitization occurs very often against the background of vaccination or when suffering from any infections.

Other possible causes of this pathology

Hemolytic disease of newborns can also develop due to:

• the presence of pathologies of the placenta. This is a special organ that appears during pregnancy and is designed to provide all nutrients to the child’s body. It also performs a protective function, preventing the mixing of the blood of the mother and fetus. When this barrier is violated, the child’s red blood cells pass into the woman’s body. Also, antibodies in the mother’s blood move to the fetus, which leads to the development of this dangerous condition;
• the presence of rather rare incompatibilities that are not related to the Rh factor or blood group;
• the risk of developing this dangerous disease in an infant increases several times if the mother has a negative Rh factor and her partner has a positive one. It is the latter that is most often transmitted to the child;
• a potential danger to the development of this pathological condition is present if a woman has blood type 2, and a man has blood type 3 or 4. This problem can also appear in other cases. For example, when the expectant mother has blood type 3, and the father has 2 or 4.

The mechanism of development of this pathological condition

During pregnancy, a woman’s body produces antibodies in small quantities to foreign fetal antigens that are of paternal origin. This process is completely natural. Under normal conditions, maternal antibodies bind to fetal antigens in the placenta and amniotic fluid.

But if sensitization was present before this or the pregnancy proceeds pathologically, what happens is completely different. The placenta cannot fully provide barrier functions and the woman’s antibodies reach the fetus. This negative process develops most during childbirth. Therefore, it is in newborns that hemolytic disease is detected.

The pathogenesis of this pathology is the development of hemolysis of red blood cells in the fetus or infant. This occurs against the background of damage to their membrane by the mother's antibodies. As a result, premature extravascular hemolysis develops. This leads to the breakdown of hemoglobin, from which bilirubin is formed.

If this process occurs very intensively (especially when the liver is immature in newborns), quite dangerous consequences are observed. Free bilirubin begins to accumulate in the child’s blood, which has a toxic effect. It is not excreted from the body along with urine, but very easily penetrates into lipid-rich tissues and organs.

These include the brain, liver, and adrenal glands. Free bilirubin disrupts many processes in tissues and leads to disruption of their functioning.

Depending on the causes of hemolytic disease of newborns, it is customary to distinguish several forms:

• a form that develops as a result of a conflict on the Rh factor;
• a form that develops against the background of a blood group conflict;
• a form that develops due to other reasons.

Depending on the clinical manifestations of hemolytic disease of newborns based on the Rh factor, etc., the following forms are distinguished:

• icteric;
• edematous;
• anemic.

Severity

Hemolytic disease of newborns can have different degrees of severity:

• light form. Its presence is determined only by the results of laboratory tests; any symptoms are either absent or mild;
• moderate form. It is characterized by an increase in the level of bilirubin in the blood, but signs of intoxication are not yet observed. In this case, jaundice develops in the first hours of the child’s life. It is accompanied by a decrease in the level of hemoglobin (less than 140 g/l), an increase in the concentration of bilirubin (more than 60 µmol/l), an enlargement of the liver and spleen;
• severe form. Accompanied by damage to the nuclei of the brain, cardiac dysfunction and respiratory dysfunction.

Symptoms of the icteric form

The icteric form of hemolytic disease is the most common. Even if a child is born at term, his liver does not function at full capacity. This organ begins its enzymatic activity only a few days after birth.

The process of destruction of red blood cells, which leads to hemolytic disease, does not begin immediately. Yellowness of the skin is detected a few hours after birth or the next day. It is very rare for a baby to be born with this problem.

In many cases, the icteric form of this pathological condition is characterized by the following symptoms:

• against the background of the destruction of red blood cells in the blood, the level of bilirubin (bile pigment) begins to increase, which leads to the coloring of the skin yellow;
• development of anemia. When performing a general blood test, a rather low level of hemoglobin is detected;
• an increase in the size of some organs (liver, spleen);
• the mucous membranes and sclera of the eyes turn yellowish;
• the appearance of lethargy, drowsiness, decreased basic reflexes and muscle tone, which worsens as the concentration of bilirubin increases;
• after a week, signs of cholecystitis are detected, the volume of bile secreted into the intestines decreases. In this case, discoloration of stool and change in urine color are also observed. The skin takes on an uncharacteristic greenish tint. This all indicates an increase in the level of direct bilirubin.

The severity of the condition of a sick child depends on whether he was born on time or earlier. The presence of concomitant infections, oxygen starvation (in utero, after birth) and many other factors is also important.

Kernicterus

On the 3rd day of a child’s life, the level of indirect bilirubin in the blood reaches its critical values. If the necessary treatment is not carried out in a timely manner, the concentration of the direct substance, which is characterized by a toxic effect on the body, also begins to gradually increase.

Kernicterus is accompanied by the destruction of brain nuclei. This condition is subject to correction only at the beginning of development. Subsequently, this cannot be influenced by any methods.

Typically, kernicterus in hemolytic disease is accompanied by the following symptoms:

• the child develops motor restlessness;
• muscle tone sharply increases;
• opisthotonus develops. It is characterized by the fact that the child takes a special convulsive position. His back is arched, his head is thrown back, his legs are extended, his arms, feet and fingers are usually bent;

• detect the “setting sun” symptom. In this case, the eyeballs move downwards, while the iris is covered by the eyelid;
• The child screams very loudly.

If a newborn survives such a serious condition, he will develop serious mental defects or cerebral palsy.

Edema form

Hydrops fetalis is quite rare, but it is considered the most dangerous among other types of this pathological condition. This problem develops due to Rh conflict between the blood of the mother and the child. Its progression begins in the womb, so a child is born with severe anemia and other pathologies.

Also, very often such a pregnancy ends in spontaneous abortion. This happens at 20 weeks or later. If the child managed to survive and was born, the following signs are observed:

• severe swelling widespread throughout the body is detected. Sometimes effusions may appear - an accumulation of fluid released from small vessels. They are most often located in the abdominal cavity, near the heart or lungs;
• anemia is observed. The level of hemoglobin and red blood cells decreases to critical levels;

• heart failure develops;
• all organs and tissues experience oxygen starvation;
• the skin is pale, waxy;
• muscle tone on the face decreases, so it takes on a rounded shape;
• all reflexes are suppressed;
• the liver and spleen are significantly increased in size;
• The belly of a newborn baby is large and barrel-shaped.

Signs of anemic form

Hemolytic disease of newborns of the anemic form is the mildest. It develops as a result of a blood group conflict or against the background of other rare conditions. Clinical symptoms of this pathology usually appear in the first days of a child’s life. They appear against the background of a gradual decrease in hemoglobin levels due to the breakdown of red blood cells.

Immediately after the birth of the child, a general blood test does not indicate the presence of pathology. A high level of reticulocytes is detected. These are young blood cells that are produced by the bone marrow. After some time, they completely disappear, which indicates the development of the disease.

As a result of this condition, the child experiences oxygen starvation. This is manifested by the fact that the newborn does not suck the breast or bottle well, slowly gains weight, is lethargic and inactive. Such a child usually has pale skin and an enlarged liver.

Diagnosis during fetal development

Diagnosis of this pathology is carried out both during pregnancy and after the birth of the child. Initially, it involves the following procedures:

• immunological examination of the mother's blood. Performed several times during pregnancy. Helps identify antibodies in the mother’s blood that indicate the development of a conflict. Based on the results obtained, a conclusion is made about the possibility of hemolytic disease of the newborn;
• ultrasound diagnostics during pregnancy. Using this procedure, you can quickly determine the condition of the placenta, the size of the liver and spleen in the fetus, which indicates the presence of hemolytic disease. The relationship between the size of the child’s chest and head is also assessed, and the presence or absence of polyhydramnios is revealed;

• cardiotocography. Allows you to determine the condition of the fetus based on its heartbeat and heart rhythm;
• amniocentesis. A complex and dangerous procedure, during which amniotic fluid is collected using a special instrument with a thin needle. The collected material is examined for bilirubin levels, on the basis of which a conclusion is made about the presence of hemolytic disease;
• cordocentesis. A complex diagnostic procedure during which cord blood is collected. It can be performed no earlier than the 18th week of pregnancy. With the development of hemolytic disease, increased bilirubin levels and decreased hemoglobin levels are detected.

Postpartum diagnosis of hemolytic disease

To confirm the development of this dangerous condition in newborns, the following diagnostic methods are used:

• an assessment is made of the child’s appearance, his behavior, etc. All forms of hemolytic disease are accompanied by characteristic symptoms that directly indicate the presence of this problem;
• the results of a general blood test reveal low levels of hemoglobin and red blood cells, and the concentration of bilirubin, on the contrary, is significantly increased;
• in the presence of this dangerous condition, dark-colored urine is detected in the newborn. When she is tested for bilirubin, the reaction is positive;
• A Coombs test is performed, which allows you to identify the presence of direct signs of hemolytic disease.

Principles of treatment of hemolytic disease

Treatment of hemolytic disease of newborns involves removing mother's antibodies and red blood cell breakdown products from the baby's bloodstream. If this is done promptly and correctly, all serious complications can be prevented. It is also necessary to take all measures to increase the number of red blood cells and hemoglobin in the blood of a sick child.

In particularly severe cases, the following treatment measures are indicated to stabilize the newborn’s condition:

• blood transfusion. It involves its removal from the child’s body with subsequent restoration of the deficiency from the donor. An effective procedure that allows you to reduce bilirubin levels and eliminate all dangerous symptoms. In this case, it is not whole blood that is to be transfused, but specially prepared red blood cells with a negative Rh factor. This helps prevent the transmission of HIV, hepatitis and other dangerous diseases;
• use of hemosorption. The newborn's blood is passed through sorbents using special devices;
• use of plasmapheresis. This procedure takes place using special equipment that collects a small volume of blood from the child’s vascular bed. Subsequently, plasma, which is the carrier of all toxic substances, is completely removed from it;
• in severe cases, newborns are given glucocorticoids for a whole week.

Treatment of mild forms of hemolytic disease

If the course of the hemolytic disease is mild and only some of its symptoms develop, the following measures are taken to stabilize the condition of the newborn:

• First of all, phototherapy is used. It consists of irradiating the child with white and blue light, which is obtained from fluorescent lamps;
• special protein preparations and glucose are administered intravenously;
• doctors prescribe liver enzyme inducers;
• to normalize metabolism and liver function, vitamins E, C, group B and other agents are used;
• if thickening of bile occurs, choleretic agents are prescribed;
• in the presence of persistent anemia, transfusions may be used.

What are the consequences of improper treatment of hemolytic disease?

With the intensive development of all negative processes in this disease, if appropriate preventive or therapeutic measures have not been taken in a timely manner, the following occurs:

• the death of the child is possible both in the womb and in the first days after birth;
• severe disability of the newborn;
• development of cerebral palsy;
• loss of hearing or vision in a child;
• delayed intellectual development;
• the appearance of psychovegetative syndrome;
• development of reactive hepatitis.

These consequences can be prevented if during pregnancy you constantly monitor the presence of antibodies in the mother’s blood and, if necessary, take all prescribed therapeutic measures.

So, we continue the story about TTH in newborns and ways to diagnose this condition before the onset of dangerous consequences and a critical moment, as well as possible measures to treat such a pathology if it suddenly happens to you and your baby. In fairness, I will immediately note that today doctors are aware of Rh conflict and are trying to do everything to prevent problems for children and mothers.

Clinic and diagnostics

We have discussed two forms of hemolytic disease of newborns, but there may also be a third form of this disease - anemic, the most favorable and mildest of all types of HDN. In terms of prognosis, it has the best prognosis; almost all children survive and develop normally. Usually the disease begins in the first week of a child’s life, but sometimes it can develop later. The pronounced pallor of the skin and mucous membranes will be striking, while the liver and spleen are usually enlarged. In the blood of children, the number of red blood cells decreases to 2-3 million against the norm of 4.5-5.5 million in 1 ml of blood, the amount of hemoglobin is usually reduced to 40-50 g/l against the normal of 110-140 g/l, while immature cells are detected in the blood forms of red blood cells that are defective in terms of their functions. Such anemia in children is considered normochromic or hypochromic (there is normal or little hemoglobin in red blood cells), with a reduced size of red blood cells. The number of leukocytes usually does not change. Sometimes the development of anemia is possible with a delay around the third week from birth and without previous jaundice and other changes.

How are such tension headaches treated?

Treatment of such pathologies should begin even before the baby is born, from the period if problems were identified earlier. If they are detected during childbirth or immediately after it, today there are many methods and approaches to treatment. But the basis of everything is active and faster actions to solve problems, otherwise developing metabolic disorders will lead to irreversible consequences. Thus, in the anemic form of HDN, successful correction of disorders can be carried out using frequent and fractional transfusions of Rh-negative blood, and this is combined with the introduction of vitamins C, group B and iron supplements after the child reaches the age of one month.

But such fractional administration of blood or red blood cells will not help with more severe forms when there is a threat of damage to the brain, kidneys or liver, and only replacement blood transfusions significantly reduce the severity of complications and mortality from. But a replacement blood transfusion will be effective only if it is used in a timely manner - it must be carried out no later than 36 hours from the moment the child is born. The main goal of replacing all the baby's blood is to remove from his body all red blood cells damaged by antibodies, which for the body are the main sources of bilirubin, which is toxic to the body. In addition, there is also an automatic removal of antibodies along with blood, as well as the removal of already formed bilirubin and toxins from all body tissues. Even if there is no severe hemolysis (destruction of red blood cells), but there is a high level of bilirubin, then a replacement blood transfusion is still performed to remove indirect bilirubin from it and detoxify the body. In the event of a conflict regarding the AB0 system, according to blood group, the child is transfused with red blood cells of the first group in half with blood plasma of the fourth, or blood plasma of the same group.

If there are high concentrations of bilirubin in the umbilical cord blood and in the presence of jaundice in a child born to a mother with Rh immunization, it is necessary to immediately begin a replacement blood transfusion. In doubtful cases, the bilirubin level is determined twice or thrice a day, and if it increases, this will also be an indication for transfusion surgery. After the first exchange transfusion operation, a special phenomenon of “ricochet” or special recoil may occur, with a secondary increase in the levels of bilirubin, which leaves the tissues and organs without having time to bind and be eliminated by the liver. The duration of such increases may vary, as may the level of bilirubin. If the replacement of red blood cells is monitored, then the amount of fetal (fetal) hemoglobin is determined before and after the transfusion, and despite the almost complete removal of the fetal red blood cells, only a certain part of the bilirubin is removed from his body, and its flow from the tissues into the blood continues for some time.

If the repeated increase in bilirubin level does not exceed the initial level that was before the transfusion, and after a few hours the bilirubin level begins to decrease, you can leave the child under observation and not transfuse red blood cells into him again. If the bilirubin level rises again, the replacement blood transfusion procedure is repeated. You should not refuse the transfusion procedure, especially if jaundice develops; this can lead to damage to brain tissue and irreversible neurological consequences. This is especially dangerous in premature infants, and they may undergo replacement blood transfusion procedures several times a day. Usually, a replacement blood transfusion is performed through the umbilical vein, placing an umbilical catheter in it, which can remain in it for up to seven days.

It is possible to perform a replacement blood transfusion through other vessels - the radial artery or the saphenous vein of the thigh, the external jugular vein. Complications from such an exchange transfusion operation are not frequent; usually the level of potassium in the blood may increase with drowsiness and muscle hypotension, changes in heart function. The doctor corrects all this. Blood is injected only at body temperature with additional heating of the child, slowly, in portions of 10-15 ml, so as not to overload his heart. Multiple blood transfusions are used to treat the edematous form of HDN, also using punctures of the cavities and removal of edematous fluid from them. If there is a threat of kernicterus, lumbar punctures may be indicated to reduce disturbances in the circulation of cerebrospinal fluid.

Today, in parallel with exchange blood transfusion, the introduction of special plasma substitutes is also used - hemodez solution, neocompensan, which can adsorb bilirubin and reduce its concentration in tissues. Also, babies are injected with an albumin solution or single-group blood plasma in the first days of HDN to bind the remaining bilirubin and neutralize it in the liver. Along with this, the babies are given glucose to nourish the tissues, since they cannot yet absorb food and need support. For liver pathology, use a heating pad on the liver area, oral magnesium solutions, and lipocaine. They help the liver function and prevent it from degenerating into fatty tissue.

If there is a mild icteric form of HDN, the child can be given phototherapy with white or blue light for three days; bilirubin decreases quite quickly and actively, and the yellow color of the skin gradually disappears. In case of severe Rh conflict and hemolytic disease, breastfeeding should be abandoned for the first ten days, since human milk contains antibodies and they can activate a new release of portions of bilirubin into the blood. Gradually, as the baby becomes better, the baby is put to the mother's breast after the mother's milk is checked for antibodies to red blood cells. They also control the bioassay - the baby is put to the breast and his hemoglobin and red blood cell levels are examined. If the indicators are normal, he continues to be fed from his mother’s breast, but if hemoglobin and red blood cells decrease, he is transferred to donor milk or artificial formula. If there are antibodies to the AB0 system in the mother's blood, breastfeeding should be abandoned - such antibodies remain in the blood plasma for a long time and they are not destroyed even when breast milk is boiled.

What could be the consequences?

Children who have suffered severe tension-type headache or jaundice during the newborn period may often remain with severe damage to the central nervous system, which is usually manifested by physical slowing in development or problems in mental development, symptoms of damage to the nuclei of the brain and ganglia with paralysis, problems with body movement, etc. d. But with timely initiation of treatment, all these consequences can be avoided if replacement blood transfusions or other methods of therapy are carried out. Only a small percentage of such children treated in time had minor developmental deviations, the rest were only slightly weakened in the first months of life. After discharge, such children are carefully monitored by a pediatrician and neurologist for the first six months, and blood conditions are regularly monitored. They often develop late anemia, which is treated with iron supplements. There may be frequent colds and allergies, diathesis and digestive problems, but all these phenomena can be corrected, and children grow up quite normal and healthy.

More articles on the topic “Myths in Pediatrics”:

Hemolytic disease of the newborn is associated with an immunological conflict between mother and fetus. It is possible when the blood of the mother and her baby does not match in some respects.

Causes of Rh conflict and blood group conflict

A pregnant woman does not have the same antigen in her blood that her fetus has (this may be a specific blood group antigen or Rh D antigen). The child receives this antigen from the father. This, for example, happens if a Rh-negative pregnant woman (who does not have Rh antigen D) carries a Rh-positive child (he has Rh antigen D received from the father), or if she is born to a mother with blood group I child with group II or III. These are the most common types of conflict. But there are also more rare cases, when the child inherits other erythrocyte antigens from the father (each of them has its own name and causes its own characteristics of the course of the disease). The expectant mother’s body begins to produce special antibody proteins against the antigen that the fetus has and that the woman herself does not have. Antibodies can begin to be produced early - even during pregnancy, or they can appear almost during childbirth. These antibodies can penetrate through the placenta to the baby. The shorter the pregnancy period at which antibodies began to be produced, the more they accumulate and the more likely the baby will become more severely ill. Since group and Rh antigens are found in red blood cells, the consequences of the conflict are reflected in them. The result of such a discrepancy is hemolysis, or the destruction of red blood cells in a fetus or already born baby under the influence of maternal antibodies. Hence the name - hemolytic disease.

What happens in the body of a fetus or newborn?

The consequences of the destruction of red blood cells (red blood cells) are the development (usually slow, gradual, but sometimes extremely rapid) of anemia in the child - a decrease in the amount of hemoglobin, as well as the appearance of jaundice. In severe cases of the disease, the baby may be born with already icteric skin color or very pale, swollen, but these cases are rare. In the vast majority of children, hemolytic disease can be suspected if jaundice begins too early or is too bright. It must be noted that the skin of many completely healthy newborns begins to acquire a yellow tint around the third day of life. And there is a physiological explanation for this: the baby’s liver is not yet fully mature, it slowly processes a pigment called bilirubin (namely, it is what causes the yellowness of the skin). Its peculiarity lies in its ability to accumulate in those body tissues that contain fat. Thus, the ideal place for bilirubin accumulation is subcutaneous fat. The brightness of the icteric shade depends on the amount of this pigment in the newborn’s body.

Physiological jaundice never appears early and goes away without treatment by about 8-10 days of life of a full-term baby. The level of bilirubin with it does not exceed 220-250 µmol/l, often being even less than the indicated figures. The child's condition does not suffer with physiological jaundice.

In the case of hemolytic disease, so much bilirubin is formed that the baby’s immature liver is not able to quickly utilize it. With hemolytic disease, there is an increased breakdown of “red” cells, and the product of hemoglobin conversion, the pigment bilirubin, accumulates in the blood. Hence the combination of anemia and jaundice in hemolytic disease.

Jaundice in hemolytic disease occurs early (possibly even on the first day of a child’s life) and persists for a long time. The liver and spleen are characterized by enlargement. The child's skin color is bright yellow, the sclera - the whites of the eyes - may be stained. If there is anemia, the baby will look pale and the jaundice may not appear as pronounced.

Jaundice can also be a manifestation of other diseases of the newborn, such as congenital liver defects, bile ducts or intrauterine infection - hepatitis. This is one of the most common signs of child distress. Therefore, only a doctor can definitely classify a particular case of jaundice in a newborn as normal or pathological.

Antigens and antibodies

The presence of certain antigens determines what blood type a person will have. So, if there are no antigens A and B in red blood cells, a person has blood type I. There is antigen A - it will have group II, B - III, and with antigens A and B at the same time - IV.

There is a balance between the content of antigens in red blood cells and the content of other special proteins (antibodies) in the liquid part of the blood - plasma. Antibodies are designated by the letters α and β. Antigens and antibodies of the same name (for example, A antigens and α antibodies) should not be present in the blood of the same person, as they begin to interact with each other, ultimately destroying red blood cells. That is why a person, for example, with blood group III has B antigen in his erythrocytes, and α antibodies in his blood plasma. Then the red blood cells are stable and can perform their main function - to carry oxygen to the tissues.

In addition to the group antigens mentioned above (i.e., those that determine membership in a certain blood group), there are many other antigens in erythrocytes. Their combination may be unique for each individual. The best known is the Rh antigen (the so-called Rh factor). All people are divided into Rh-positive (their red blood cells contain the Rh antigen, designated Rh antigen D) and Rh-negative (do not have this antigen). The first are the majority. Naturally, there should be no anti-Rh antibodies in their blood (by analogy with antibodies for blood groups), otherwise red blood cells will be destroyed.

How to assess the likelihood of hemolytic disease?

The most important thing is timely monitoring of the pregnant woman in the antenatal clinic. It is at this stage that a whole series of studies can be carried out to confirm or exclude Rh conflict. The most famous study is the detection of antibodies against fetal red blood cells in the blood of a pregnant woman. Their increase with the duration of pregnancy or, even worse, a wave-like change in level (either high, then low or not detectable at all) allows us to suspect a more serious prognosis for the child and forces us to change the tactics of examination and treatment of the expectant mother. In addition, methods of ultrasound diagnostics of the condition of the fetus and placenta, obtaining a sample of amniotic fluid, testing fetal blood obtained from the umbilical cord, etc. are used.

Manifestations of hemolytic disease

As a rule, a blood type conflict occurs quite easily for a baby.

With Rh conflict, there are a greater number of cases in which manifestations are pronounced and treatment is required. In addition, the prenatal onset of the disease, when already at birth the child has certain signs of it, is the prerogative of Rh conflict.

If the disease began inside the mother's womb, the baby, usually premature, may be born with edema and severe anemia. If the conflict manifests itself in the child only after birth (there were no signs of intrauterine suffering), then it causes the occurrence of the already mentioned anemia and jaundice. Jaundice is still a more common sign of conflict. If it is very pronounced (and, accordingly, the level of bilirubin is pathologically high), there is a risk of damage to the child’s central nervous system.

As mentioned above, bilirubin can accumulate in body tissues that contain fat. It's good if it's subcutaneous tissue. It’s worse when there is so much bilirubin in the blood that it begins to penetrate certain structures of the brain (primarily the so-called “subcortical nuclei”), since they also contain fatty inclusions. Normally, when the level of bilirubin circulating in the blood is low, this does not happen.

For each child, the critical level of bilirubin, above which neurological disorders can be predicted, is individual. At high risk are those infants whose jaundice (including as a manifestation of hemolytic disease) has developed against an unfavorable background. For example, they were born premature or experienced oxygen deficiency in the prenatal period, did not immediately breathe on their own after birth, which required resuscitation measures, were cooled, etc. There are quite a few of these factors, and pediatricians take them into account when deciding on treatment tactics and predicting outcomes.

Possible consequences of hemolytic disease

As a result of the action of bilirubin on the central nervous system (on the “subcortical nuclei”), “kernicterus” can occur - a condition that is reversible with proper treatment only at its very beginning. If, nevertheless, brain damage occurs, then after a few weeks obvious long-term consequences develop, when a lag in the child’s psychomotor development, partial or complete loss of vision or hearing, and the occurrence of repeated seizures or obsessive movements in the baby are noted. And it is impossible to return such a child to full health.

It should be noted that such an unfavorable course of the disease with obvious consequences is extremely rare, only with a combination of significant destruction of red blood cells that began in utero and, as a consequence, a rapid rise in bilirubin levels in the newborn. A bilirubin level exceeding 340 µmol/l is considered potentially dangerous for full-term infants.

Less pronounced consequences concern the risk of developing anemia in the first year of life in a child who has had hemolytic disease. A reduced amount of hemoglobin during anemia causes insufficient oxygen supply to the baby’s organs, which is undesirable for a growing organism. As a result, the child may appear pale, tire quickly, and be at greater risk of illness, such as a respiratory infection.

The current level of development of medicine, correct diagnostic and treatment tactics make it possible to avoid the pronounced consequences of hemolytic disease of newborns. The vast majority of cases of the disease have a favorable course.

Who is at risk?

The disease can occur in fetuses and newborns if their mothers are Rh negative or have blood type I.

Let us first consider the variant of conflict based on blood type. The laws of inheritance suggest the possibility of giving birth to a woman with blood group I of a child with group II or III. It is in this case that incompatibility due to the group factor may arise. But “can” does not mean “should.” Not every case of the given potentially unfavorable combination of blood groups of mother and child will lead to undesirable consequences. In principle, it is quite difficult to give a 100% forecast of whether such a conflict will arise. Other factors need to be taken into account. The simplest, perhaps, is the blood group of the child’s father. If the father has blood group I, then it is clear that hemolytic disease of the newborn due to the group factor does not threaten their baby. After all, if mom and dad have blood group I, then their baby will also have group I. Any other blood group of the father will be fraught with potential danger.

In the case of Rh incompatibility (the mother is Rh negative and the child is Rh positive), the disease can occur if the mother has a repeat pregnancy and the birth of this Rh positive baby was preceded by childbirth or cases of another pregnancy outcome (for example, abortions, miscarriages, frozen pregnancy). That is, the very fact that a woman has had a previous pregnancy in her life, during which antibodies could have already formed, is significant. During the next pregnancy, there are more antibodies - they accumulate. But one should not think that the fate of having a hemolytic disease awaits every child of an Rh-negative mother. Too many factors contribute to the possibility of this disease occurring. It is worth mentioning at least the possibility of predicting the Rh status of the unborn child. If both mom and dad are Rh-negative, the baby is not afraid of the disease, because he will definitely also be Rh-negative. A baby with Rh-negative blood can be born to a mother of the same Rh-negative type if the father is Rh-positive. In this case, the father, being Rh positive, does not inherit the Rh antigen D to him: according to the laws of inheritance of traits, this is quite possible.

Therefore, one can only guess whether the future child will be Rh-positive, having received Rh antigen D from the father, or Rh-negative, having not received the corresponding antigen.

Currently, it is possible to determine the probability of having a Rh-positive or Rh-negative child in a married couple, where the woman is Rh-negative and the man is Rh-positive. The necessary detailed analysis of the Rh factor is usually carried out in special laboratories (for example, at blood transfusion stations).

Necessary examinations

In case of childbirth in a Rh-negative woman or a woman with blood type I, a small amount of blood is taken from the umbilical cord vein for testing. As a result, the child’s blood type and Rh are determined, as well as the level of bilirubin in the umbilical cord blood. If necessary, a repeated study of the bilirubin level may be prescribed in the future, as well as a general blood test (it allows you to diagnose anemia). During treatment, the bilirubin level is monitored as often as required by the individual characteristics of the development of the disease in the child: usually - once a day or in two days. But there are times when control is required several times during one day.

If there is a suspicion of hemolytic disease, then to confirm the diagnosis, a blood test of the child and mother is prescribed for the so-called compatibility, in other words, it is determined whether there are antibodies in the mother’s blood that can destroy the child’s red blood cells.

Features of feeding a child with physiological jaundice

It is important to emphasize that children with jaundice resulting from hemolytic disease must receive adequate nutrition, otherwise bilirubin levels may increase. Therefore, these children need more frequent and prolonged breastfeeding. There is no need to fear that the antibodies contained in milk will aggravate the situation, since under the influence of the aggressive environment of the stomach, the antibodies in the milk are almost immediately destroyed. The diagnosis of hemolytic disease itself is not a contraindication to breastfeeding. But the possibility and method of feeding breast milk (suckling from the breast or feeding with expressed milk) is determined by the doctor, based on the condition of the child. If the child's condition is severe, he can receive nutrition in the form of solutions injected into a vein.

Treatment of physiological jaundice in newborns

The best way to treat the icteric form (and it is the most common in this disease) is light therapy (or phototherapy). If severe jaundice occurs, the baby is placed under a special lamp. Phototherapy lamps look different, but most of them look like long fluorescent lamps. Often parents and doctors say; "The child is sunbathing." In fact, just the opposite. Under the influence of the light of these lamps, his skin becomes discolored, its yellowness noticeably decreases. This happens because the pigment bilirubin leaves the subcutaneous fat. It simply becomes water-soluble and in this state can be excreted in the child’s urine and feces.

The baby can receive phototherapy both in the neonatal department and in the maternal ward if his condition is not severe and he is breastfed. This method, which allows not to separate mother and baby, is preferable, but this is only possible if appropriate equipment is available in the postpartum wards.

If the child’s condition requires it, he may be prescribed intravenous administration of glucose and other solutions. An indication for intravenous infusion may be a high level of bilirubin, as well as the baby’s inability to receive the required amount of milk through the mouth. The volume missing from the normal physiological fluid requirement is administered intravenously.

The most severe forms of the disease, accompanied by massive destruction of red blood cells under the influence of maternal antibodies and, as a consequence, severe jaundice and anemia, require blood transfusions. This type of transfusion is called an exchange transfusion. The child’s blood, containing red blood cells ready for destruction, is almost completely replaced by carefully selected donor blood, which will be resistant to the action of maternal antibodies, since it does not contain the “problematic” antigen. So, for an exchange transfusion, Rh-negative blood is taken for an Rh-positive child, which means that as a result of the transfusion, Rh-positive red blood cells will not enter his body, which can be destroyed by antibodies circulating in his blood. He will receive Rh-negative red blood cells that are resistant to maternal antibodies. Sometimes the particular severity of the disease requires multiple exchange transfusions for the newborn.

The timing of treatment for hemolytic disease varies from person to person. Most mild cases of the disease end by the 7-8th day of the child’s life: it is until this time that the baby can receive phototherapy. If his condition is good, he is discharged home. But cases with prolonged intense jaundice, difficult to respond to phototherapy, or hemolytic disease with complications (or in combination with other significant pathology) require further examination and treatment in a children's hospital.

Modern medical care technologies also involve treating an unborn baby. If during pregnancy the diagnosis of hemolytic disease of the fetus is confirmed, severe anemia is detected (and this is possible and, first of all, relevant for Rh incompatibility) and there is a danger to the health and even the life of the child, then a blood transfusion is given to the fetus even before birth. Under ultrasound control, a long needle is used to puncture the vein of the fetal umbilical cord and carefully selected donor red blood cells are injected into it. Of course, this tactic is not used in ordinary maternity hospitals.

Prevention of physiological jaundice in newborns

Is it possible to prevent the occurrence of the disease? It is difficult to answer this question in the affirmative if the mother and child are incompatible by blood type. But the prevention of Rh conflict has long been known and is even indicated in special regulatory documents.

It is divided into nonspecific and specific. The first implies the prevention of abortion, miscarriage, i.e. other outcomes of the first pregnancy in Rh-negative women, other than childbirth. Simply put, for an Rh-negative woman, it is important that there are no cases of termination of pregnancy before the birth of the child, since each of them can increase the chance of the formation of antibodies and, therefore, the birth of an affected child. Of course, such a woman can also give birth to a Rh-negative (and therefore without hemolytic disease) child. But preventing abortions, due to their undeniable harm to health, will never be superfluous.

Specific prevention consists of administering to a Rh-negative woman after her first abortion or miscarriage a special drug - anti-Rhesus immunoglobulin. It will protect the baby, which the mother will bear during a subsequent pregnancy, from antibodies, simply by not allowing them to form. Thus, protection is provided from the antibodies of the unborn child (which she will probably want to give birth to after a certain time).

When the first pregnancy of an Rh-negative woman ends in childbirth, the Rh status of the child is determined. If the baby is Rh positive, the woman is also given immunoglobulin. If the newborn is Rh negative, immunoglobulin is not prescribed, because antibodies in this case cannot be formed.

Modern methods involve the administration of immunoglobulin to a Rh-negative woman during pregnancy. If the child’s father is Rh-positive and no antibodies are found in the pregnant woman’s blood, then at 28 and 34 weeks she can be given anti-Rh immunoglobulin. For this, it is not necessary to determine the Rh status of the fetus.

erythroblastosis fetalis

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

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

When can pathology occur?

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

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

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

Manifestations of different forms of hemolytic disease of newborns

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

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

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

Edema

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

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

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

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

Jaundice

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

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

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

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

Anemic

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

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

Therapy

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

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

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

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

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

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

Treatment with traditional medicine

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

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

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

Prevention

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

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

The point of the procedure is that immunoglobulins capture Rh proteins from the blood of a “positive” baby, preventing them from entering the “negative” circulatory system of the mother. If there is no mixing of different types of blood, antibodies to the child’s blood will not form in the mother’s blood.

Long-term consequences

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

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

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

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