Blood transfusion for hemolytic disease: is it necessary for a child? Hemolytic disease of the newborn (HDN): causes, risks, manifestations, treatment Appendix A3. Related documents

In case of hemolytic disease, which is possible in a child in the presence of a conflict with the mother's body by blood group or Rh factor, urgent help is needed. Toxic bilirubin, produced in quantities that the baby's enzyme systems simply cannot cope with, negatively affects the nervous tissue and leads to jaundice, so it is important to establish the correct diagnosis as soon as possible and determine the scope of emergency care and further treatment tactics.

Modern clinics have all the conditions for carrying out intrauterine and postnatal diagnostics of this pathology in a child. Antenatal determination of the risk of hemolytic disease of the newborn (HDN) is carried out at the initial stages of gestation in all women at high risk. This category includes all expectant mothers with an Rh negative factor who have had multiple abortions, miscarriages, stillbirths, and blood transfusions.

In a future mother with a negative rhesus, the appearance and level of anti-rhesus antibodies are determined in the laboratory during the entire gestation period, for which blood is regularly taken for analysis. In the case of a sharp increase in titer, we can talk about a high probability of developing HDN.

In order to clarify or confirm the diagnosis, amniocentesis is carried out according to strict indications - the collection and study of amniotic fluid with the determination of the presence of bilirubin, some biochemical parameters. Indirectly, signs of HDN formation can be seen during ultrasound examination, which will include:

• Thickening in the placenta, an increase in its volume and edema;
• Development of polyhydramnios;
• Increased size and circumference of the baby's tummy.

Clinical symptoms, blood tests in a child

After childbirth, the diagnosis in a child will be carried out on the identification of clinical manifestations - the formation of jaundice, anemic syndrome, an increase in the size of the liver and spleen. Laboratory indicators are extremely important, which must be taken into account in a complex over time. In order to determine bilirubin, the blood of the newborn is taken and examined. Its high rates in the first days after childbirth and a rapid increase in concentration indicate a massive destruction of red blood cells. Toxic bilirubin in such quantities is dangerous, so the child is placed in the intensive care unit and urgent medical measures are taken.

The main requirements for the treatment of HDN are an integrated approach and the timeliness of all measures taken. Regardless of the form of the disease in the treatment of hemolytic disease, it is necessary to adhere to the following principles:

• To direct all efforts to relieve the intoxication of the newborn, to eliminate jaundice and in the shortest possible time;
• Do everything possible to remove the mother's antibodies from the child's body, which will contribute to the destruction of red blood cells, which causes jaundice and intoxication to increase;
• To carry out therapy, which will be aimed at improving the functional state of organs and systems, initially it is about the work of the liver and kidneys.

Blood transfusion as a treatment

Among the effective methods of treatment include exchange blood transfusion, which is carried out as early as possible after birth. Methods such as hemosorption or plasmapheresis are not excluded. Blood transfusion allows you to get rid of excess bilirubin and maternal antibodies, in addition, it seems possible to compensate for the deficiency of protein and erythrocytes. Today, it is not blood as such with plasma and corpuscles that is transfused, but plasma separately or in combination with erythrocyte mass.

If there is a question about blood transfusion, it will be shown:

• if the concentration of indirect bilirubin rises above the critical figures;
• if the hourly stay of bilirubin exceeds certain norms;
• with pronounced symptoms of anemia, when the hemoglobin index is less than 98 g / l of blood.

With a mild form of HDN, they adhere to a conservative treatment method, which will be aimed at lowering the amount of bilirubin in the baby - transfusion of protein solutions, glucose, the introduction of certain medications, and so on.

A fairly effective method of treatment, which will be aimed at reducing the level of dangerous bilirubin - irradiation of the baby with blue light (phototherapy method). The baby is placed in a special incubator with a radiation source. In it he spends a certain amount of time. To date, it has been proven that feeding a child with donor milk is not justified due to fear of a rise in bilirubin levels. The baby can breastfeed, the antibodies in the milk will not harm the baby. All of the mother's antibodies will die when the acid in the baby's stomach interacts.

What to do to prevent pathology

Any disease is more expedient and easier to prevent than to cure. It is this rule with the risk of developing HDN that must be strictly adhered to. It is much better and more effective to prevent the development of pathology than to treat it, sometimes unsuccessfully. We must not forget about the high infant mortality rate. As a preventive measure, women with a negative Rh factor are injected with anti-Rh-gamma-immunoglobulin immediately after the birth of their first Rh-positive baby. This method of prevention is also carried out for women after abortion. Thanks to the introduction of serum, antibodies to the fetal erythrocytes will be removed from the mother's blood, and, therefore, the production of Rh antibodies will stop.

The desensitization method can also be used, which is achieved by replanting a skin flap from the husband. In addition, it is necessary to exclude abortions, especially when the first pregnancy occurs, because most of the first babies are born healthy.

Weight (gr)

Phototherapy should be discontinued when the level of indirect bilirubin drops below 170 μmol / L.

Unfortunately, the water-soluble derivative is unstable. In the dark, this isomer can spontaneously convert back to the toxic and water-insoluble isomer. Another undesirable effect is a decrease in the level of albumin in the blood plasma, riboflavin, vitamin E., in connection with which vitamin B2 is prescribed for prophylaxis in a daily dose of 0.5 mg / kg.

Prophylactic use of vitamin E is also necessary, especially for premature babies, in whom the decrease in its level persists for more than 3 weeks.

Complications of phototherapy can be; overheating, dehydration, loose green stools, erythematous rash, less often - a kind of skin pigmentation ("bronze child syndrome"), anemia due to impaired absorption of iron and a decrease in the level of vitamins E and B2. Children with heart failure may develop shock.

When signs of cholestasis appear, the fraction of direct bilirubin increases by 20-30%, the time of phototherapy should be limited to 6-12 hours a day or canceled in order to avoid the development of the "bronze child" syndrome.

Infusion therapy

Infusion therapy is carried out for the purpose of detoxification and can be started at various times from the onset of the disease.

The calculation of fluid requirements for a newborn, provided that enteral nutrition is maintained, is presented in Table 7.

Phototherapy requires an increase in the volume of infusion therapy: for newborns weighing 1500 g or less, an additional 0.5 ml / kg / h, and over 1500 g - 1 ml / kg / h. When carrying out IT, the child's weight should be monitored, diuresis, the level of electrolytes, blood sugar, Ht should be assessed.

Infusion therapy includes transfusion of 10% glucose (dextrose) solution, and with a tendency towards critical bilirubin levels, fresh frozen plasma, especially in immature, premature infants; from the 2nd day of life, it is possible to administer plasma (10-15 ml / kg of body weight) or 5% albumin (1 g / kg / day). The selection of a blood group depending on the type of conflict is described in detail in the ZPK section.

Infusion therapy is carried out intravenously (into the umbilical cord vein, subclavian vein, peripheral veins) or intragastrically through a gastric tube. The rate of intravenous administration in full-term newborns can reach 7-10 ml / h, in premature infants - 6-8 ml / h.

Intragastric drip of fluids.

Intragastric administration of fluid can be started from 3-4 days of life, at the rate of 60-70 ml / kg of body weight. It is carried out using a 5% glucose solution (dextrose), to prevent the development of cholestasis, a 25% solution of magnesium sulfate (25% solution of 5 ml / kg, during the day), drotaverin (2% solution of 0.5 ml / kg, during the day), potassium chloride solution (4% solution 5 ml / kg, during the day).

Glucose is a substrate from which ATP is formed in erythrocytes - a macroerg, which supplies energy for many biochemical and transport processes in erythrocytes. Infusion of magnesium sulfate solution can also significantly prolong the life of red blood cells (especially in children with hypomagnesemia). The previously used antioxidant therapy (mainly Vit. B) is currently not recommended, since it causes additional suppression of the pathologically reduced level of LPO-AOA. With intragastric fluid administration, there is no need to reduce the feed volume.

Immunoglobulin therapy

Immunoglobulin is injected with the aim of blocking Fc receptors, as a result of which it becomes impossible for the antigen to interact with the antibody, which prevents hemolysis. An intravenous immunoglobulin is used. An early start of administration is necessary: \u200b\u200bthe first 2 hours of life (with antenatal diagnosis of HDN) or later, but immediately upon diagnosis.

Due to the small number of randomized studies conducted, at present, drug administration schemes have not been fully developed. Normal human immunoglobulins are used. Possible application schemes:

Normal human immunoglobulin IV 1 g / kg every 4 hours, 1 day or

Normal human immunoglobulin IV 500 mg / kg every 2 hours, 1 day or

Normal human immunoglobulin intravenously 500 mg / kg, once, 1 day or

Normal human immunoglobulin IV 500-750 mg / kg every 2-4 hours until the level of bilirubin decreases or

Normal human immunoglobulin IV 800 mg / kg 1 time per day, 3 days.

Regardless of the dose and frequency, a positive effect (95%) was obtained, which manifested itself in a significant decrease in the frequency of PPC and the duration of phototherapy.

Medicines that activate the enzyme systems of the liver.

Phenobarbitalat present, it is practically not used due to the fact that the onset of the effect is significantly delayed, from the moment of its application, and against the background of use, an increase in the syndrome of depression from the central nervous system (lethargy, respiratory and sucking disorders) is noted. However, in cases of severe jaundice in a child in the absence of depression syndrome, it is possible to use phenobarbital by mouth at 5-10 mg / kg 1-3 times / day, 5 days or more.

Cordiamine(inside a 25% solution of 2-3 drops on glucose in a daily dose of 60 mg / kg) is able to induce in the liver the activity of enzymes involved in the biotransformation of various chemicals. It activates the centers of the medulla oblongata, mainly respiratory and vasomotor. With the introduction of cordiamine per os in a daily dose of 60 mg / kg, divided into 8 doses, a state of anxiety arises in newborns. This effect is used to eliminate the inhibitory effect of phenobarbital on the respiration of newborns, as well as to enhance its ability to reduce the level of bilirubin in the blood plasma.

Preparations that adsorb bilirubin in the intestine.

The attitude towards the appointment of drugs in this group is not unambiguous. It is believed that a cleansing enema in the first 2 hours of life or suppositories with glycerin lead to early discharge of meconium, reliably reduce the severity of the maximum rise in the blood NB level. These activities are carried out for all children with jaundice at birth. However, after 12 hours of life, such treatment has no effect. To reduce the likelihood of developing high hyperbilirubinemia, increase the effectiveness of phototherapy and reduce its duration, cholesteramine (1.5 g / kg of body weight), agar-agar (0.3 g / kg per day) are prescribed in the first day of life. In order to have a faster bowel movement and reduce the absorption of bilirubin from the intestine, a 12.5% \u200b\u200bsolution of magnesium sulfate, or a solution of xylitol and sorbitol, is also prescribed internally. Also, adsorbents are prescribed inside - activated carbon, carbolene, 100 mg (0.1) 3 times a day in the form of a 10% solution per os on glucose. The drug "Smecta" is widely used. The appointment of magnesium sulfate (inside in the form of a 12.5% \u200b\u200bsolution, 1 teaspoon 3 times a day) promotes the flow of indirect bilirubin into the intestine and its excretion with feces. It should be remembered that all these remedies are symptomatic and are used in addition to the main treatment.

Replacement blood transfusion (BTC).

Distinguish between early (first 2 days of life) and later (from the third day of life) ZPC.

Indications to early ZPKagainst the background of ongoing infusion therapy and phototherapy:

The level of total bilirubin in the umbilical cord blood is over 80 μmol / l,

Full-term newborns have an hourly increase in total bilirubin of more than 6.8 μmol / l;

Premature newborns have an hourly increase in total bilirubin of more than 5.1 μmol / L

Indication for late ZPKare the numbers of indirect bilirubin:

For a full-term newborn - 308-340 μmol / l.

For a premature newborn, the critical bilirubin figures are presented in table 8.

Clinical symptoms depend on the form of the disease.

• The edematous form (or dropsy of the fetus) is rare.
  • It is considered the most severe form among others.
  • As a rule, it begins to develop even in utero.
  • Miscarriages are common in early pregnancy.
  • Sometimes the fetus dies late or is born in a very serious condition with widespread edema, severe anemia (decreased hemoglobin (a blood dye that carries oxygen) and red blood cells per unit volume of blood), oxygen deprivation, heart failure.
  • The skin of such a newborn is pale, waxy. The face is rounded. Muscle tone is sharply reduced, reflexes are depressed.
  • The liver and spleen are significantly enlarged (hepatosplenomegaly). The belly is large, barrel-shaped.
  • Characterized by widespread tissue edema, sometimes with effusion (accumulation of fluid that came out of small vessels) into the abdominal cavity, cavities around the heart (pericardial) and lungs (pleural). This is due to increased capillary permeability (the thinnest vessels in the body) and a decrease in total protein in the blood (hypoproteinemia).
• The anemic form is the most favorable form downstream.
  • Clinical symptoms appear in the first days of a child's life.
  • Anemia, pallor of the skin and mucous membranes, enlargement of the liver and spleen in size gradually progresses.
  • The general condition suffers slightly.
• The icteric form is the most common form. Its main symptoms are:
  • jaundice (yellow coloration of body tissues due to excessive accumulation of bilirubin (bile pigment) and its metabolic products in the blood);
  • anemia (decreased hemoglobin (blood dye that carries oxygen) and red blood cells per unit volume of blood);
  • hepatosplenomegaly (enlargement of the liver and spleen in size).
• Jaundice develops in the first 24 hours after the birth of a child, less often on the second day, has a progressive course.
  • The skin of such a patient is yellow with an orange tint.
  • Visible mucous membranes and sclera turn yellow.
  • The earlier jaundice appears, the more severe the disease progresses.
  • As the level of bilirubin in the blood increases, children become lethargic, sleepy; they have decreased reflexes and muscle tone.
  • On days 3-4, the level of indirect bilirubin (bile pigment formed as a result of the breakdown of hemoglobin and did not have time to pass through the liver) reaches a critical value (more than 300 μmol / l).
  • Symptoms of nuclear jaundice appear (damage to the subcortical nuclei of the brain with indirect bilirubin):
    • motor restlessness;
    • stiff neck muscles (a sharp increase in muscle tone);
    • opisthotonus (convulsive posture with a sharp arching of the back, throwing the head back (resembles an arc with support only on the back of the head and heels), stretching the legs, bending the arms, hands, feet and fingers);
    • symptom of the "setting sun" (the movement of the eyeballs is directed downward, while the iris is covered by the lower eyelid). All this is accompanied by a squeak and a strong cry (“cerebral” shrill cry).
  • By the end of the week, against the background of massive decay of red blood cells, the release of bile into the intestine decreases (bile thickening syndrome) and signs of cholestasis (bile stagnation) appear: the skin becomes greenish-dirty, the feces become discolored, the urine darkens, the level of direct bilirubin (bilirubin which passed through the liver and was rendered harmless).

Forms

Depending on the type of immunological conflict, the following forms are distinguished:

• hemolytic disease of the newborn (HDN) due to the conflict on the Rh factor;
• hemolytic disease of the newborn (HDN) due to a conflict on the blood group (ABO incompatibility);
• rare factors (conflict over other antigenic systems).

Clinical forms:

• edematous;
• icteric;
• anemic.

According to the severity, the following forms of the disease are distinguished.

• Mild form: diagnosed in the presence of moderately expressed clinical and laboratory or only laboratory data.
• Moderate form: there is an increase in the level of bilirubin in the blood, but there are no bilirubin intoxication and complications yet. This form of the disease is characterized by jaundice, which appeared in the first 5-11 hours of a child's life (depending on the Rh-conflict or AB0-conflict), the hemoglobin level in the first hour of life is less than 140 g / l, the level of bilirubin in the blood from the umbilical cord is more than 60 μmol / l, enlarged liver and spleen.
• Severe form: it includes the edematous form of the disease, the presence of symptoms of damage to the brain nuclei with bilirubin, respiratory and cardiac dysfunction.

The reasons

The cause of hemolytic disease of newborns is the incompatibility of the blood of the mother and the fetus, most often for the Rh factor, less often for group antigens (ABO systems) and only in a small percentage of cases for other antigens.

• Rh-conflict occurs when a developing fetus in a Rh-negative woman has Rh-positive blood.
• Immune conflict according to the ABO system develops with O (I) blood group in the mother and A (II) or B (III) in the fetus.
• A child is born sick only if the mother was previously sensitized (already has an increased sensitivity to blood components that she has encountered earlier).
• An Rh-negative woman can be sensitized by transfusion of Rh-positive blood even in early childhood; with miscarriage, especially with induced abortion.
• The most common cause of sensitization (an increase in the body's sensitivity to the effects of any factor in the environment or internal environment) is childbirth. Therefore, the first child is in a much more favorable position than subsequent children.
• When a conflict develops according to the ABO system, the number of previous pregnancies does not matter, since in ordinary life, sensitization (hypersensitivity to agents foreign to the body) to antigens A and B occurs very often (for example, with food, during vaccination, some infections).
• A significant role in the development of hemolytic disease is played by the placenta (a special organ that communicates between the body of the mother and the child during pregnancy). If its barrier function is disturbed, the transition of red blood cells of the fetus into the bloodstream of the mother and the mother's antibodies to the fetus is facilitated.
• Along with erythrocytes, foreign proteins (Rh factor, antigens A and B) enter the mother's body.
  • They cause the formation of Rh antibodies or immune antibodies (anti-A or anti-B) that cross the placenta into the fetal bloodstream.
  • Antigens and antibodies combine on the surface of erythrocytes, form complexes that destroy them (hemolysis of erythrocytes of the fetus and newborn).
• As a result of the pathological breakdown of red blood cells in the blood of the fetus, the level of indirect (unconjugated) bilirubin increases, and anemia develops.
• Unconjugated bilirubin has a toxic effect on brain cells, causing significant changes in them up to necrosis.
• At a certain concentration (over 340 μmol / L in term infants and over 200 μmol / L in deeply premature infants), it can penetrate the blood-brain barrier (physiological barrier between the circulatory system and the central nervous system) and damage the subcortical nuclei of the brain and cortex, which leads to to the development of nuclear jaundice.
• This process is aggravated by a decrease in the level of albumin (blood protein), glucose, with the use of certain drugs, such as steroid hormones, antibiotics, salicylates, sulfonamides.
• As a result of toxic damage to liver cells, direct bilirubin appears in the blood (rendered harmless by the liver).
• Cholestasis (stagnation of bile) occurs in the bile ducts, the secretion of bile into the intestine is disturbed.
• With anemia (a decrease in hemoglobin (a blood dye that carries oxygen) and red blood cells per unit volume of blood), new foci of hematopoiesis arise due to hemolysis of erythrocytes.
• Erythroblasts (young forms of erythrocytes) appear in the blood.

Diagnostics

Antenatal (prenatal) diagnosis of a possible immune conflict is required.

• Obstetric-gynecological and somatic history: the presence of miscarriages, stillbirths, deaths of children in the first day after birth from jaundice, blood transfusion without taking into account the Rh factor.
• Determination of rhesus and blood group of mother and father. If the fetus is Rh-positive, and the woman is Rh-negative, then she is at risk. In the case of a marriage of a man who is homozygous (in the hereditary set of which pairs of chromosomes carry the same form of a given gene) for the Rh factor, and a Rh negative woman, all children will be carriers of a positive Rh factor. However, in a heterosite (that is, with a heterogeneous genotype (hereditary basis)) father, half of the offspring inherits a negative Rh factor. Also at risk are women with blood group I.
• Determination of the titer of anti-Rh antibodies in dynamics in a Rh-negative woman (at least three times during pregnancy).
• Trasabdominal amniocentesis at 34 weeks of gestation (puncture of the fetal bladder through the abdominal wall to extract amniotic fluid for diagnostic purposes) in case of establishing the risk of immune conflict. Determine the optical density of bilirubin, antibodies in the amniotic fluid.
• Ultrasound during pregnancy. With the developing hemolytic disease of the fetus, there is a thickening of the placenta, its accelerated growth due to edema, polyhydramnios (excessive accumulation of amniotic fluid), an increase in the size of the abdomen of the fetus due to an enlarged liver and spleen.
• Postnatal (postpartum) diagnosis of hemolytic disease of the newborn is based on:
  • clinical manifestations of the disease at birth or soon after:
    • jaundice: the skin and visible mucous membranes are yellow, feces are discolored, dark urine;
    • anemia: pallor of the skin;
    • enlarged liver and spleen (hepatosplenomegaly);
    • signs of kernicterus: stiff neck muscles (a sharp increase in muscle tone), opisthotonus (convulsive posture with a sharp arch of the back, with the head tilting back (resembles an arc with support only on the back of the head and heels), stretching the legs, bending the arms, hands, feet and fingers );
    • the symptom of the "setting sun" (the movement of the eyeballs is directed downward, while the iris is covered by the lower eyelid);
  • laboratory data:
    • decrease in hemoglobin levels below 150 g / l;
    • a decrease in the number of red blood cells;
    • an increase in the number of erythroblasts and reticulocytes (young precursors of erythrocytes);
    • an increase in the level of bilirubin in the blood of the umbilical cord is more than 70 μmol / l, in the rest of the blood - 310-340 μmol / l. An increase in bilirubin in the blood of a newborn with hemolytic disease by 18 μmol / l every hour;
    • urine is dark in color, gives a positive reaction to bilirubin;
    • it is important to study incomplete antibodies using the Coombs test.

Incomplete antibodies are maternal antibodies that penetrate the placenta, which, although attached (adsorbed) to the surface of fetal red blood cells, do not adhere the red blood cells to each other (agglutination). If such erythrocytes are combined with Coombs' serum, which contains antibodies, then agglutination occurs (adhesion of spectrocytes and their precipitation). This is a positive direct Coombs test.

Treatment of hemolytic disease of the newborn

• In severe cases of hemolytic disease of the newborn, resort to:
  • replacement blood transfusion (bloodletting followed by donor blood transfusion);
  • hemosorption (passing blood in a special apparatus through sorbents (activated carbon or ion-exchange resins), which are capable of absorbing toxic substances));
  • plasmapheresis (taking a certain amount of blood using a special apparatus and removing the liquid part from it - plasma, which contains toxic substances).
• Replacement blood transfusion allows you to remove indirect (toxic bilirubin that did not pass through the liver) bilirubin and mother's antibodies from the child's blood, as well as replenish the deficiency of red blood cells. Use Rh-negative blood of the same group as the child's blood.
• At present, due to the danger of HIV transmission, hepatitis is not transfused with whole blood, but with Rh-negative erythrocyte mass (these are erythrocytes remaining after removing most of the plasma from preserved blood) with fresh frozen plasma (liquid blood component).
• If hemolytic disease of newborns is caused by group incompatibility, then the erythrocyte mass of group 0 (I) is used, and plasma is either AB (IV) group, or single-group in a volume of 180-200 ml / kg. This is enough to replace about 95% of a newborn's blood.
• Indications for replacement blood transfusion in the first day of life in full-term newborns are as follows:
  • the concentration of indirect bilirubin in the umbilical cord blood is more than 60 μmol / l;
  • an increase in the concentration of indirect (unbound) bilirubin per hour more than 6-10 μmol / l;
  • the concentration of unconjugated bilirubin in the peripheral blood is more than 340 μmol / l;
  • hemoglobin less than 100 g / l.
• Newborns born in critical condition are immediately given glucocorticoids within a week.
• With a mild form of this disease or after surgical treatment, conservative methods are used:
  • intravenous infusion of protein drugs, glucose;
  • appointment of inducers of microsomal liver enzymes;
  • vitamins C, E, group B, cocarboxylase, which improve liver function and normalize metabolic processes in the body.
• With the syndrome of thickening of bile, cholagogues are prescribed internally. In severe anemia, transfusion (transfusion) of erythrocyte mass or washed erythrocytes is performed.
• At the same time, phototherapy is prescribed (irradiation of the newborn's body with a fluorescent lamp with white or blue light). Photooxidation of indirect bilirubin, which is in the skin, occurs with the formation of water-soluble substances, which are excreted in urine and feces.

Complications and consequences

In severe cases of this disease, the prognosis is poor. Often occurs:

• perinatal (from 28 weeks of gestation to 7 days after birth) fetal death;
• disability;
• cerebral palsy is a symptom complex of motor disorders, accompanied by a change in muscle tone (more often an increase in tone);
• complete hearing loss (hearing loss);
• blindness;
• delayed psychomotor development;
• reactive hepatitis (liver inflammation) against the background of bile stagnation;
• psychovegetative syndrome - a mental disorder (anxiety, depression appears) against the background of this disease.

Prevention of hemolytic disease of the newborn

Prevention is divided into specific and non-specific.

• Non-specific is the correct blood transfusion with the obligatory consideration of the blood group and Rh factor and the preservation of pregnancies.
• Specific prevention consists in the introduction of anti-D immunoglobulin in the first 24-48 hours after childbirth (in case the mother is Rh negative, and the fetus is Rh positive) or abortion.
• If the antibody titer rises during pregnancy, then resort to:
  • methods of detoxification using hemosorption (passing blood in a special apparatus through sorbents (activated carbon or ion-exchange resins) that are capable of absorbing toxic substances);
  • 3-4 times intrauterine replacement blood transfusion at 27 weeks of gestation with washed erythrocytes of 0 (I) group Rh-negative blood with subsequent delivery, starting from the 29th week of pregnancy.

Additionally

Fetal erythrocytes may differ in their properties from the mother's erythrocytes.

• If such erythrocytes penetrate the placenta (the main organ that communicates the body of the mother and the fetus), they become foreign agents (antigens), and in response to them, the mother's body produces antibodies (blood proteins that are formed as a result of the introduction of other substances into the body, including bacteria, viruses, toxins).
• The penetration of these antibodies into the fetus can cause:
  • hemolysis (breakdown of erythrocytes);
  • anemia (decreased hemoglobin (blood dye that carries oxygen) and red blood cells per unit volume of blood);
  • extremely dangerous jaundice (yellow staining of body tissues due to excessive accumulation of bilirubin (bile pigment) and its metabolic products in the blood).

	137 μmol / l	171 μmol / l	171 μmol / l	171 μmol / l	171 μmol / l
	171 μmol / l	171 μmol / l	171 μmol / l	257 μmol / l	257 μmol / l
	205 μmol / l	257 μmol / l	257 μmol / l	257 μmol / l	257 μmol / l
	257 μmol / l	257 μmol / l	257 μmol / l	257 μmol / l	274 μmol / l
	257 μmol / l	274 μmol / l	274 μmol / l	291 μmol / l	291 μmol / l
	296 μmol / l	308 μmol / l	308 μmol / l	308 μmol / l	310 μmol / l
	308 μmol / l	310 μmol / l	315 μmol / l	320 μmol / l	340 μmol / l

In the presence of risk factors for the development of bilirubin encephalopathy, PPC is performed at lower bilirubin levels. These factors include:

Apgar score at 5 minutes< 3 балла.

Hypoproteinemia (total serum protein< 50 г/л).

Hypoglycemia (< 2,2 ммоль/л).

The presence of a generalized infectious disease.

When the first symptoms of bilirubin intoxication appear, immediate PPC is indicated, regardless of the bilirubin level.

The choice of drugs for ZPC.

In an isolated Rh-conflict, Rh-negative erythrocyte mass (washed thawed erythrocytes) and fresh frozen plasma (AB (IV) plasma may be used) are used with the child's blood. Do not make PPC Rh-positive erythrocytes.

In an isolated group conflict, erythrocyte mass (washed thawed erythrocytes) of group 0 (I) is used, which coincides in terms of the Rh factor with the Rh factor of the child's erythrocytes, and plasma AB (IV) or one group with the child's blood group. Erythrocytes of the child's blood group should not be used for PPC.

If both Rh incompatibility and incompatibility in the AB0 system are possible, as well as after intrauterine blood transfusions, Rh negative erythrocyte mass (washed thawed erythrocytes) of group 0 (1) and plasma AB (IV) or one group with the blood group of the child is used for PPC ...

When HDN with a conflict for rare factors, donor blood (washed, thawed erythrocytes) is used, which does not have a "conflict" factor.

Calculation of the volume of drugs for ZPK.

The total volume is 1.5-2 BCC, i.e. for a full-term baby - about 150 ml / kg, for a premature baby - about 180 ml / kg. The ratio of erythrocyte mass (washed thawed erythrocytes) and plasma depends on the initial level of Hb before the operation. The total volume includes the volume of red blood cells (washed thawed erythrocytes) required to correct anemia, and the volume of red blood cells (washed thawed red blood cells) and plasma required to achieve the PPC volume. The volume of erythrocyte mass (washed, thawed erythrocytes) required to correct anemia is calculated by the formula:

Number of ml ores mass \u003d (160 - Hb (g / l) child) x 0.4 x child's weight (kg).

The volume of erythrocyte mass (washed thawed erythrocytes) required to correct anemia should be subtracted from the total volume, and the remaining volume is replenished with erythrocyte mass (washed thawed erythrocytes) and plasma in a 2: 1 ratio. The above corresponds approximately to the following ratio of erythrocyte mass (washed thawed erythrocytes), depending on the level of Hb in a child:

ZPK technique.

The ZPC is passed through one of the large vessels (umbilical vein, subclavian vein). Before the PPC, blood is taken to determine the level of bilirubin, the compatibility of the blood of the donor and recipient. ZPK is carried out in a "pendulum manner", i.e. withdrawing and injecting alternately a portion of blood at the rate of 5-7 ml / kg of the child's weight. Before the onset of ZPC, it is possible to administer plasma at the rate of 5 ml / kg of body weight. ZPK is started with blood elimination. Before the onset of the ZPC and throughout it, the catheter is flushed with heparin solution. With an initial Hb level below 80 g / L, the PAD begins with anemia correction, i.e. introduction of only erythrocyte mass (washed thawed erythrocytes) under the control of the level of Hb. After reaching the level of Hb 160 g / l, erythrocyte mass (washed thawed erythrocytes) and fresh frozen plasma are injected. To do this, you can dilute the erythrocyte mass (washed thawed erythrocytes) with plasma, or you can alternately inject 2 syringes of erythrocyte mass (washed thawed erythrocytes) and 1 syringe of plasma. At the end of the ZPC, blood is taken again to determine the level of bilirubin. After ZPC, conservative therapy is continued.

CPD may be accompanied by the development of immediate and delayed side effects (Table 9)

Correction of anemia.

In case of severe (Hb level less than 100 g / l) anemia detected after birth, PCP is performed. If the level of Hb immediately after birth is 100-140 g / l, correction of anemia is indicated. Selection of drugs and technique is the same as described above (see "Replacement blood transfusion").

Late anemia develops 2–3 weeks after PPC. Usually hyporegenerative and hypoerythropoietic in nature. For its correction, recombinant erythropoietin alpha s / c 200 IU / kg 1 r / 3sut, 4-6 weeks is used.

If iron deficiency is detected during therapy with recombinant erythropoietin, iron preparations are connected to therapy: iron sulfate (in drops or syrup) or iron (III) hydroxide polymaltose (in drops) inside at the rate of 2-4 mg of elemental Fe / kg 1 r / day, 4-6 weeks.

Forecast

With the edematous form, the prognosis is less favorable, due to the severity of the child at birth. With an icteric form, the prognosis is determined by the degree of damage to the central nervous system. With anemic form, the prognosis is most favorable.

Perinatal mortality in HDN is 2.5%. The overwhelming majority of the mental and psychomotor development of children who underwent HDN corresponds to the age norms. Lagging in physical development is noted in 4.9% of children. CNS pathology is detected in about 8% of children.

Prevention.

Numerous scientific studies have shown that the problem of having children with hemolytic disease cannot be solved only by improving methods of its diagnosis and treatment. Indeed, it is possible to reduce perinatal morbidity and mortality through large-scale preventive measures:

Strict accounting of Rh-affiliation during blood transfusions;

Prevention of abortion among Rh-negative women.

Specific prevention of Rh sensitization by administering anti-Rh immunoglobulin after any termination of pregnancy (childbirth, induced and spontaneous abortions, ectopic pregnancy) in the absence of a Rh antibody titer. The drug is administered within 2 hours (maximum 48 hours) after childbirth, 1 dose (300 mcg), during surgical interventions (caesarean section, manual separation of the placenta) and with premature placental abruption, the dose is doubled. For abortions and ectopic pregnancy - immediately after the end of the operation.

Thanks to specific prophylaxis in developed countries, the problem of Rh incompatibility has been practically solved. Unfortunately, in Russia, due to insufficient provision of medical institutions, anti-Rh-immunoglobulin after the end of pregnancy is not administered to all Rh-negative patients, so the problem of immunological conflict for our country is still relevant.

Dispensary observation.

During the dispensary observation of children who have undergone HDN, several groups of possible complications should be considered:

1.neurological (diffuse symptoms);

2. hematological (development of late anemia by the 2nd month of life);

3. otorhinolaryngological (hearing loss);

4. hepatogenic (in children treated with PPC, hepatitis may develop in 1-1.5%);

5. allergic (often severe forms of atopic dermatitis);

6. speech therapy.

In practical work, it must be remembered that hematopoiesis is disturbed not only in newborns with hemolytic disease, but also in children without signs of the disease, born to women with Rh sensitization. Newborns born with Rh sensitization in the mother,should be allocated to a group during dispensary observation, threatened with respect to the development of anemia.

The pediatrician monitors the child in the first half of the year at least 1 time per month. A general blood test is performed once a week, but at least 3 times a month. Long-term preventive therapy with iron preparations at the rate of 2 mg / kg per day. Medical withdrawal from preventive vaccinations up to 1 year or more, especially after PPC. BCG is not performed in the maternity hospital and is postponed up to 6 months. An iron diet is recommended for the mother during lactation.

Educational and methodological material:

Hemolytic disease of the newborn (HDN) - a pathological condition of the newborn, accompanied by massive breakdown of erythrocytes, is one of the main causes of the development of jaundice in newborns.

Hemolytic disease of the newborn is diagnosed in 0.6% of newborns. Hemolytic disease of newborns manifests itself in 3 main forms: anemic, icteric, edematous.

HEMOLYTIC DISEASE OF THE NEWBORN

Hemolytic disease of the newborn (morbus haemoliticus neonatorum) - hemolytic anemia of newborns caused by the incompatibility of the blood of the mother and the fetus for the Rh factor, blood group and other blood factors. The disease is observed in children from the moment of birth or is detected in the first hours and days of life.

Hemolytic disease of the newborn, or fetal erythroblastosis, is one of the most serious diseases of children of the neonatal period. Arising in the antenatal period, this disease can be one of the causes of spontaneous abortions and stillbirths. According to the WHO (1970), hemolytic disease of newborns is diagnosed in 0.5% of newborns, the mortality rate from it is 0.3 per 1000 live births.

Etiology, causes of hemolytic disease of the newborn.

The cause of hemolytic disease of newborns became known only at the end of the 40s of the XX century. in connection with the development of the doctrine of the Rh factor. This factor was discovered by Landsteiner and Wiener in 1940 in the Macacus rhesus monkeys. Later, these same researchers found that the Rh factor is present in the erythrocytes of 85% of people.

Further studies showed that hemolytic disease of newborns can be caused by incompatibility of the blood of the mother and the fetus, both in terms of the Rh factor and in the blood group. In rare cases, the disease occurs as a result of incompatibility of the blood of the mother and fetus for other blood factors (M, N, M5, N3, Rell, Kidd, Luis, etc.).

The Rh factor is found in the stroma of erythrocytes. It has no connection with gender, age and belonging to the ABO and MN systems. There are six main antigens of the rhesus system, inherited by three pairs of genes and denoted either C, C, D, d, E, e (according to Fischer), or rh ", hr", Rh 0, hr 0, rh ", hr" (according to Winner). In the development of hemolytic disease of the newborn, the most important is the D-antigen, which is absent in the mother and is present in the fetus as a result of its inheritance from the father.

Hemolytic disease of the newborn, caused by incompatibility in the ABO system, is more common in children with blood groups A (II) or B (III). The mothers of these children have 0 (I) blood group, which contains agglutinins α and β. The latter can block fetal red blood cells.

It was found that mothers whose children were born with manifestations of hemolytic disease, in most cases, even before the onset of this pregnancy, were sensitized to erythrocyte antigens of this fetus due to previous blood transfusions, as well as pregnancies with a Rh-positive fetus.

Currently, there are three types of Rh antibodies that form in the sensitized body of people with Rh negative blood: 1) complete antibodies, or agglutinins, 2) incomplete, or blocking, 3) latent.

Complete antibodies are antibodies capable of causing agglutination of erythrocytes specific for a given serum through normal contact; this reaction does not depend on the salt or colloidal state of the medium. Incomplete antibodies can cause agglutination of erythrocytes only in a medium containing high molecular weight substances (serum, albumin, gelatin). Latent Rh antibodies are found in very high concentrations in human serum with Rh negative blood.

In the occurrence of hemolytic disease of newborns, the most important role belongs to incomplete Rh antibodies, which can easily penetrate the placenta into the fetus due to their small molecule size.

Pathogenesis. Development of hemolytic disease of newborns

The normal course of pregnancy provides for the synthesis by a woman of antibodies to genetically foreign antigens of the fetus of paternal origin coming to her. It was found that in the placenta and amniotic fluid, maternal antibodies bind to fetal antigens. With previous sensitization, with a pathological course of pregnancy, the barrier functions of the placenta are reduced, and maternal antibodies can reach the fetus. This happens most intensively during childbirth. Therefore, hemolytic disease of the newborn usually begins after birth.

In the pathogenesis of hemolytic disease, the occurrence of hemolysis of erythrocytes in a fetus or a newborn child due to damage to the membrane of red cells by maternal antibodies is of primary importance. This leads to premature extravascular hemolysis. During the breakdown of hemoglobin, bilirubin is formed (35 mg of bilirubin is formed from each gram of hemoglobin).

Intensive hemolysis of erythrocytes and enzymatic immaturity of the liver of the fetus and newborn child lead to the accumulation of free (indirect) bilirubin in the blood, which has toxic properties. It is insoluble in water, not excreted in the urine, but easily penetrates into lipid-rich tissues: the brain, adrenal glands, liver, disrupting the processes of cellular respiration, oxidative phosphorylation and transport of certain electrolytes.

A severe complication of hemolytic disease is nuclear jaundice (kernicterus), caused by the toxic effect of indirect bilirubin on the nuclei of the base of the brain (subthalamic, hippocampus, striatal body, cerebellum, cranial nerves). The occurrence of this complication is facilitated by prematurity, acidosis, hypoalbuminemia, infectious diseases, as well as a high level of indirect bilirubin in the blood (more than 342 μmol / l). It is known that at a serum bilirubin level of 342-428 μmol / l, nuclear jaundice occurs in 30% of children.

In the pathogenesis of hemolytic disease of newborns, a dysfunction of the liver, lungs, and the cardiovascular system plays a certain role.

Symptoms Flow. The clinical picture of hemolytic disease of the newborn.

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

The edematous form is the most severe. It is characterized by pronounced edema with accumulation of fluid in the cavities (pleural, abdominal), pallor of the skin and mucous membranes, a significant increase in the size of the liver and spleen. Some newborns have slight bruising and petechiae.

Large changes are observed in the composition of peripheral blood. In such patients, the amount of hemoglobin is reduced to 30-60 g / l, the number of erythrocytes often does not exceed 1x10 12 / l, anisocytosis, poikilocytosis, polychromasia, normo- and erythroblastosis are expressed; the total number of leukocytes is increased, neutrophilia is noted with a sharp shift to the left. Anemia in such children is so severe that, in combination with hypoproteinemia and damage to the capillary wall, it leads to the development of heart failure, which is considered the main cause of death before the birth of a child or soon after.

The icteric form is the most common clinical form of hemolytic disease of the newborn. The first symptom of the disease is jaundice that occurs on the 1-2nd day of life. The intensity and shade of jaundice gradually change: first orange, then bronze, then lemon and, finally, the color of unripe lemon. There is an icteric staining of the mucous membranes, sclera. The size of the liver and spleen increases. In the lower abdomen, tissue is pasty. Children become lethargic, adynamic, suck poorly, their reflexes of newborns are reduced.

Examination of peripheral blood reveals anemia of varying severity, pseudo-leukocytosis, which occurs due to an increase in young nucleated red cells, which are perceived in Goryaev's chamber as leukocytes. The number of reticulocytes increases significantly.

For the icteric form of hemolytic disease of newborns, an increase in the level of indirect bilirubin in the blood is characteristic. Already in the umbilical cord blood, its level may be higher than 60 μmol / L, and later it reaches 265-342 μmol / L and more. There is usually no clear connection between the degree of yellowness of the skin, the severity of anemia and the severity of hyperbilirubinemia, but it is believed that the yellowness of the palms indicates a bilirubin level of 257 μmol / L and higher.

Severe complications of the icteric form of hemolytic disease of newborns are damage to the nervous system and the development of nuclear jaundice. When these complications occur, the child first appears to have increasing lethargy, decreased muscle tone, absence or inhibition of the Moro reflex, regurgitation, vomiting, and pathological yawning. Then the classic signs of nuclear jaundice appear: muscle hypertension, stiff neck muscles, forced position of the body with opisthotonus, stiff extremities, hands clenched into a fist, a sharp "cerebral" cry, hypersthesia, bulging fontanelle, twitching of the facial muscles, convulsions, symptom "Setting sun", nystagmus, symptom of Graefe; apnea periodically occurs.

Another relatively common complication is bile thickening syndrome. Its signs are discolored stools, saturated color of urine, enlarged liver. When studying blood, an increase in the level of direct bilirubin is found.

The anemic form is observed in 10-15% of patients with hemolytic disease of newborns. Its early and persistent symptoms should be considered a general pronounced laxity and pallor of the skin and mucous membranes. Pallor is clearly revealed by the 5-8th day after birth, since at first it is masked by a slight yellowish. An increase in the size of the liver and spleen is observed.

In peripheral blood with this form, the content of hemoglobin is reduced to 60-100 g / l, the number of erythrocytes is in the range of 2.5x10 12 / l-3.5x10 12 / l, normoblastosis and reticulocytosis are observed. Bilirubin levels are normal or moderately elevated.

The diagnosis of hemolytic disease of newborns is based on anamnesis data (sensitization of the mother due to previous blood transfusions; the birth of children in this family with jaundice, their death in the neonatal period; indications of the mother about the late miscarriages, stillbirths that she had earlier), on the assessment of clinical symptoms and laboratory data. The latter are of leading importance in the diagnosis of the disease.

First of all, the blood group and Rh-belonging of the mother and child are determined, the content of reticulocytes in the peripheral blood and the level of bilirubin in the venous blood of the child are examined.

In case of Rh incompatibility, the titer of Rh antibodies in the mother's blood and milk is determined, a direct Coombs test is performed with the child's erythrocytes and indirectly with the mother's blood serum. In case of incompatibility according to the ABO system in the mother's blood and milk, the titer of a- or p-agglutinins in salt and protein media is determined. Immune antibodies in a protein medium have a titer four times higher than in a salt medium. These antibodies belong to class G immunoglobulins and cross the placenta, causing the development of hemolytic disease of the newborn. The direct Coombs' reaction in ABO incompatibility is usually negative.

If the clinical and laboratory data clearly indicate hemolysis, and the blood of the mother and the child are compatible by the Rh factor and the ABO system, then it is advisable to put the Coombs reaction, conduct a test for the individual compatibility of the mother's blood and the child's erythrocytes, look for antibodies to anti-genes, rarely causing hemolytic disease of newborns: c, d, e, Kell, Diffy, Kidd.

For antenatal diagnostics, the prognostic value is the determination of bilirubin in the amniotic fluid at a gestational age of 32-38 weeks: with an optical spectrophotometric density of amniotic fluid (with a filter of 450 nm) 0.15-0.22 units. a mild form of hemolytic disease of newborns develops, above 0.35 units. - severe form. The edematous form of hemolytic disease of newborns in the antenatal period can be diagnosed using ultrasound.

The determination of the titer of Rh antibodies in the blood of pregnant women contributes to the identification of women sensitized to Rh antigens. However, the degree of increase in the titer of rhesus antibodies in the blood of a pregnant woman does not always correspond to the severity of hemolytic disease. The jumping titer of Rh antibodies of a pregnant woman is considered to be prognostically unfavorable.

Diagnostics. Differential diagnosis of hemolytic disease of the newborn.

Hemolytic disease of newborns has to be differentiated from a number of diseases and physiological conditions. First of all, it is necessary to establish the hemolytic nature of the disease and exclude hyperbilirubinemia of hepatic and mechanical origin.

Among the causes of the appearance of jaundice of the second group in newborns, the most important are congenital diseases of an infectious nature: viral hepatitis, syphilis, tuberculosis, listeriosis, toxoplasmosis, cytomegalovirus infection, as well as sepsis acquired not only in utero, but also after birth.

Common signs of jaundice in this group are the following: the absence of signs of hemolysis (anemia, signs of irritation of the red line of hematopoiesis, an increase in the level of indirect bilirubin, an enlarged spleen) and an increase in the level of direct bilirubin.

It should also be remembered that obstructive jaundice may occur in newborns, which usually appears due to an anomaly in the development of the biliary tract - agenesis, atresia, stenosis and cysts of the intrahepatic bile ducts. In these cases, jaundice usually appears by the end of the 1st week, although it can appear in the first days of life. It progressively intensifies, and the skin takes on a dark green, and in some cases, brownish tint. The feces may be lightly colored. With abnormalities in the development of the biliary tract, the amount of bilirubin in the blood serum is very high, it can reach 510-680 μmol / L due to an increase in direct bilirubin. In severe and advanced cases, indirect bilirubin can also increase due to the impossibility of conjugating it due to the overflow of liver cells with bilirubin of bile. The urine is dark and stains the diapers yellow. Cholesterol and alkaline phosphatase are usually elevated. The liver and spleen are enlarged and thicken with increased jaundice. Gradually, children develop dystrophy, signs of hypovitaminosis K, D and A appear. Biliary cirrhosis of the liver develops, from which children die before reaching the age of 1 year.

With a high level of indirect bilirubin in the blood and in the absence of other signs of increased hemolysis of erythrocytes, a suspicion of the conjugative nature of jaundice arises. In such cases, it is advisable to investigate the activity of lactate dehydrogenase and its first fraction, hydroxybutyrate dehydrogenase, in the child's blood serum. With hemolytic disease of newborns, the level of these enzymes is sharply increased, and with conjugational jaundice, it corresponds to the age norm.

We must not forget about the existence of a rather rare disease known as Krigler-Najar syndrome (Krigler and Najar). This is non-hemolytic hyperbilirubinemia, accompanied by the development of kernicterus. The disease is inherited in an autosomal recessive manner. Boys get sick more often than girls.

At the heart of the Crigler-Nayyar syndrome is a sharp disturbance in the formation of bilirubindiglucoronide (direct bilirubin) due to the complete absence of UDP-glucoronyl transferase, which conjugates bilirubin. The main symptom of the disease is jaundice, which appears in the first day after birth and grows intensively, holding on throughout the child's life. Jaundice is associated with a sharp increase in the blood of indirect bilirubin, the amount of which very quickly reaches 340-850 μmol / l. Against the background of a sharp increase in the blood of indirect bilirubin, symptoms of nuclear jaundice develop. Anemia is not observed. The number of young forms of erythrocytes is not increased. The amount of urobilin in the urine is within normal limits. Bile is devoid of direct, conjugated bilirubin. The defeat of the central nervous system leads to the death of the child in the first months of life. Children rarely live to be 3 years old.

Hereditary hemolytic anemias are diagnosed on the basis of (specific morphological signs of erythrocytes, measuring their diameter, osmotic resistance, studies of the activity of erythrocyte enzymes (primarily glucose-6-phosphate dehydrogenase, etc.), types of hemoglobin.

Treatment of hemolytic disease of the newborn.

Treatment of hemolytic disease of newborns with a high level of indirect bilirubin can be conservative or operative (replacement blood transfusion operation).

Adequate nutrition is essential for newborns with hemolytic disease.

Conservative treatment of hemolytic disease of the newborn includes the following measures:

1. measures aimed at reducing hemolysis due to stabilization of the erythrocyte membrane (intravenous infusion of 5% glucose solution, the appointment of ATP, erevita);
2. therapy that accelerates the metabolism and excretion of bilirubin from the body (taking phenobarbital at a rate of up to 10 mg / kg per day, divided into three doses, by mouth);
3. the appointment of substances that adsorb bilirubin in the intestine and accelerate its excretion with feces (agar-agar, 0.1 g three times a day by mouth; 12.5% \u200b\u200bsolution of xylitol or magnesium sulfate by mouth, 1 teaspoon three times a day or allochol on "/ 2 crushed pills also three times a day inside);
4. the use of means and measures to reduce the toxicity of indirect bilirubin (phototherapy); Recently, there have been reports of effectiveness in combating the toxic effect of indirect bilirubin of low doses of ultraviolet radiation.

Fluid therapy is helpful. The volume of infusion therapy is as follows: on the first day - 50 ml / kg and then add 20 ml / kg per day, bringing it to 150 ml / kg by the 7th day.

The composition of the infusion solution: 5% glucose solution with the addition of 1 ml of 10% calcium solution for every 100 ml, from the second day of life - 1 mmol of sodium and chlorine, from the third day - 1 mmol of potassium. Infusion rate - 3-5 drops per minute. The addition of a 5% albumin solution is shown only to children with infectious diseases, premature babies, when hypoproteinemia is detected (below 50 g / l). Infusion of hemodez and rheopolyglucin in hemolytic disease of newborns is not indicated.

Replacement blood transfusion is carried out according to certain indications. An absolute indication for replacement blood transfusion is hyperbilirubinemia above 342 μmol / L, as well as the rate of increase in bilirubin above 6 μmol / L in 1 hour, its level in umbilical cord blood is above 60 μmol / L.

Indications for replacement blood transfusion in the first day of life are anemia (hemoglobin less than 150 g / l), normoblastosis and proven incompatibility of the blood of the mother and the child by group or Rh factor.

In case of Rh-conflict, blood of the same group as in the child is used for replacement blood transfusion, Rh-negative no more than 2-3 days of conservation, in an amount of 150-180 ml / kg (with an indirect bilirubin level of more than 400 μmol / l - in a volume of 250-300 ml / kg). In case of ABO conflict, blood transfusion of group 0 (I) with a low titer of a- and ß-agglutinins, but in an amount of 250-400 ml; in this case, as a rule, the next day it is necessary to make a repeated replacement transfusion in the same volume. If the child has a simultaneous incompatibility for resuz- and ABO-antigens, then the child needs a blood transfusion of 0 (I) group.

When carrying out a replacement blood transfusion, a catheter is inserted into the umbilical vein to a length of not more than 7 cm. The blood must be warmed up to a temperature of at least 28 ° C. The stomach contents are sucked off before the operation. The procedure begins with the removal of 40-50 ml of the child's blood, the amount of injected blood should be 50 ml more than that removed. The operation is carried out slowly (3-4 ml per 1 min), the withdrawal and administration of 20 ml of blood alternate. The duration of the entire operation is at least 2 hours. It should be remembered that for every 100 ml of injected blood, 1 ml of a 10% solution of calcium gluconate must be injected. This is done to prevent citrate shock. In 1-3 hours after replacement blood transfusion, the blood glucose level should be determined.

Complications of replacement blood transfusion include: acute heart failure with the rapid introduction of large amounts of blood, cardiac arrhythmias, transfusion complications with improper selection of a donor, electrolyte and metabolic disorders (hyperkalemia, hypocalcemia, acidosis, hypoglycemia), hemorrhoids -gia syndrome, thrombosis and embolism, infectious complications (hepatitis, etc.), necrotizing enterocolitis.

After replacement blood transfusion, conservative therapy is prescribed. An indication for repeated replacement blood transfusion is the rate of increase in indirect bilirubin (replacement blood transfusion is indicated when the rate of increase in bilirubin is more than 6 μmol / l per hour).

To carry out a replacement blood transfusion, you must have the following set of instruments: sterile polyethylene catheters No. 8, 10, a button probe, scissors, two surgical forceps, a needle holder, silk, four to six syringes with a capacity of 20 ml and two or three syringes with a capacity of 5 ml, two glasses of 100-200 ml.

The technique of catheterization of the umbilical vein is as follows: after processing the operating field, the end of the umbilical cord is cut across at a distance of 3 cm from the umbilical ring; the catheter is inserted with careful rotational movements, directing it after passing the umbilical ring up along the abdominal wall, towards the liver. If the catheter is inserted correctly, then blood is released through it.

Prevention of hemolytic disease of the newborn.

The basic principles of prevention of hemolytic disease of newborns are as follows. Firstly, given the great importance of previous sensitization in the pathogenesis of hemolytic disease of newborns, each girl should be treated as a future mother, and therefore girls need to carry out blood transfusions only for health reasons. Secondly, an important place in the prevention of hemolytic disease of newborns is given to work on educating women about the harm of abortion. To prevent the birth of a child with hemolytic disease of the newborn, all women with Rh-negative blood factor are recommended to administer anti-O-globulin in an amount of 250-300 μg on the first day after an abortion (or after childbirth), which contributes to the rapid elimination of the child's red blood cells. from the mother's blood, preventing the synthesis of Rh antibodies by the mother. Thirdly, pregnant women with a high titer of anti-Rhesus antibodies are hospitalized for 12-14 days in antenatal departments at 8, 16, 24, 32 weeks, where they receive nonspecific treatment: intravenous infusion of glucose with ascorbic acid, cocarboxylase, rutin, vitamin E, calcium gluconate, oxygen therapy are prescribed; with the development of the threat of termination of pregnancy, progesterone is prescribed, endonasal electrophoresis of vitamins B 1, C. 7-10 days before delivery, the appointment of phenobarbital 100 mg three times a day is indicated. Fourthly, with an increase in the titers of anti-Rhesus antibodies in a pregnant woman, delivery is carried out ahead of schedule at 37-39 weeks by means of a cesarean section.

Consequences and prognosis in hemolytic disease of the newborn.

Hemolytic disease of the newborn: the consequences can be dangerous, up to the death of the child, the function of the liver and kidneys of the child can be impaired. Treatment should be started immediately.

The prognosis of hemolytic disease of newborns depends on the form of the disease and the adequacy of the preventive and therapeutic measures taken. Patients with edematous form are not viable. The prognosis for icteric form is favorable, provided that adequate treatment is carried out; the prognostically unfavorable development of bilirubin en-cephalopathy and nuclear jaundice, since the percentage of disability is very high in the group of such patients. The anemic form of hemolytic disease of newborns is prognostically favorable; in patients with this form, self-healing is observed.

The modern level of development of medicine, correct diagnostic and therapeutic tactics allow avoiding the pronounced consequences of hemolytic disease of newborns.

doctor of Medical Sciences, Nikolay Alekseevich Tyurin et al., Moscow (as amended by the MP website)

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