Hemolytic disease of newborns

Hemolytic disease of the newborn and fetus is an isoimmune hemolytic anemia that occurs when the mother's and fetus's blood is not compatible with erythrocyte antigens, while the antigens are the erythrocytes of the fetus, and the antibodies to them are produced in the mother's body. Hemolytic disease of newborns is diagnosed in approximately 0.6% of children. Perinatal mortality 2.5%.

[1], [2], [3], [4], [5]

What causes hemolytic disease of the newborn?

The emergence of an immune conflict, underlying the hemolytic disease of the newborn, is possible if the mother is antigen-negative, and the fetus is antigen-positive. With the development of GHP and Rh by the Rhesus factor, the erythrocytes of the mother are Rh-negative, and the fetus is Rh-positive; contain the O-factor. Implementation of the conflict (development of GBPiN) is usually carried out with repeated pregnancies, since previous sensitization is necessary.

Hemolytic disease of newborns by group incompatibility develops at 0 (1) blood group in the mother and A (II) or, less commonly, in (III) blood group in the fetus. Implementation of the conflict is possible already at the first pregnancy. GBPiN can also occur when incompatible with other rare antigenic systems: Kell, Lutheran, and others.

How does the hemolytic disease of newborns develop?

For the development of hemolytic disease of the newborn, antigen-positive erythrocytes of the fetus must enter the bloodstream of the antigen-negative pregnant woman. It is not so much the fact of the transplacental transition of the fetal erythrocytes as the quantity of fetal blood entering the mother's body that is of great importance. Factors contributing to isoimmunization, especially the Rh factor, are:

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

At the heart of the disease is hemolysis (destruction) of erythrocytes, caused by the incompatibility of blood of the mother and fetus by the Rh factor, the group and other factors of the blood that occurs on the 3-4th month of intrauterine development and sharply increases after birth.

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

The Rhesus antigenic system consists of six main antigens: C, c, D, d, E and e. Rhesus-positive red blood cells contain the D-factor, and Rhesus-negative red blood cells do not contain it, although they often display other antigens of the Rh system. Penetrated into the bloodstream Rh-negative pregnant fetus erythrocytes having D-antigen, lead in the first pregnancy to synthesis first Rh antibodies belonging to class M immunoglobulins that do not penetrate the placenta. Then, immunoglobulins of class G, capable of overcoming the placental barrier, are produced. Because of the small number of red blood cells of the fetus and immunosuppressive mechanisms, the primary immune response in a pregnant woman is reduced. That is why the implementation of the conflict with Rh-incompatibility during the first pregnancy is almost not happening, and the baby is born healthy. With repeated pregnancies, the development of conflict is possible, and the baby is born with hemolytic disease of newborns.

A- and B-antigens are located on the outer surface of the plasma membrane of the erythrocyte. Isoimmune anti-A and anti-B group antibodies belong to the class IgG, in contrast to the natural group antibodies - ayr, which belong to the IgM class. Isoimmune antibodies can bind to the corresponding antigens A and B and be fixed on other tissues, including placenta tissues. That is why the hemolytic disease of newborns according to the ABO system can develop already at the first pregnancy, but only in about 10% of cases.

If it is possible to implement both variants of the conflict, a conflict over the AB (0) system is more likely.

But not only the Rh factor is the cause of the disease. It can occur with incompatibility of blood and other factors. In addition, hemolytic disease of the fetus may occur if the blood of the mother and fetus does not match the main blood groups of the AB0 system. Antigens A and B, inherited from the father, can cause the formation of incomplete agglutinins in the mother with blood group 0, which, in contrast to conventional α- and β-agglutinins, can pass through the placental barrier and cause hemolysis of the fetal erythrocytes. Conflict on the basis of discrepancy in the AB0 system occurs in 10% of cases and proceeds, as a rule, benignly. It should be noted that the discrepancy between fetal and maternal blood 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 swelling form of hemolytic disease of newborns

The edematous form, or hydrocephalus of the fetus, occurs if the hemolysis begins still in utero, approximately from 18-22 weeks of pregnancy, has an intense character and leads to the development of severe fetal anemia. As a result, severe fetal hypoxia occurs, which causes deep metabolic disturbances and damage to the vascular wall. Increased permeability of the vascular wall leads to the fact that albumin and water are transferred from the fetal blood to the interstitial tissues. Simultaneously, the synthesis of albumin in the liver of the baby decreases, which aggravates hypoproteinemia.

As a result, a common edematous syndrome is formed in utero, ascites develops, fluid accumulates in the pleural cavities, in the pericardial cavity, etc. Reduction of the drainage function of the lymphatic system aggravates the development of ascites and accumulation of fluid in other body cavities. 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 the organs and pronounced fibrosis in the liver, hepato- and splenomegaly is formed. Ascites and hepatosplenomegaly cause high diaphragm standing, which leads to lung hypoplasia. The increased amount of indirect bilirubin produced during haemolysis is excreted from the blood and tissues of the fetus through the placenta into the mother's body, therefore there is no jaundice at birth.

Pathogenesis in icteric form of hemolytic disease of newborns

The icteric form of the disease develops if the hemolysis begins shortly before the birth. As a result of destruction of erythrocytes, the concentration of indirect (unconjugated) bilirubin is rapidly and significantly increased, 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 the accumulation of indirect bilirubin in the nuclei of the base of the brain, which leads to its defeat with the development of neuronal necrosis, gliosis and the formation of bilirubin encephalopathy (nuclear jaundice);
• increasing the load on the glucuronyltransferase of the liver, which leads to the depletion of this enzyme, the synthesis of which begins in the liver cells only after birth, and as a result, hyperbilirubinemia is maintained and intensified;
• increase in the excretion of conjugated (direct) bilirubin, which can lead to a violation of bile excretion and the development of complication - cholestasis.

As well as with edematous form, hepatosplenomegaly develops.

Pathogenesis of the anemic form of hemolytic disease

The anemic form develops when the fetus enters the bloodstream shortly before the birth of small amounts of maternal antibodies. In this case, hemolysis is not of an intensive nature, and the liver of the newborn is quite active in withdrawing indirect bilirubin. Anemia predominates, and jaundice is absent or minimal. Characterized by hepatosplenomegaly.

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 peculiarities.

Pith form

The most severe form of hemolytic disease of the newborn. The clinical picture, in addition to the above symptoms, is characterized by a widespread edema syndrome: anasarca, ascites, hydropericardium, etc. Perhaps the emergence of hemorrhages on the skin, the development of DIC syndrome as a consequence of hypoxia, hemodynamic disorders with cardiopulmonary insufficiency. They note the expansion of the heart's borders, the muffledness of its tones. Often after birth, respiratory distress develops against a background of lung 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 the pallor of the skin and visible mucous membranes, usually a very mild and moderate increase in the spleen and liver, also note jaundice of a predominantly warm yellow hue. At the birth of a child, the amniotic fluid, the umbilical cord, and the original grease can be painted.

Characteristic of the early development of jaundice: it occurs either at birth, or in the first 24-36 hours of life of the newborn.

By severity of jaundice, three degrees of icteric form of hemolytic disease of the newborn are distinguished:

• light: jaundice appears at the end of the first or the beginning of the second day of the child's life, the bilirubin content in the cord blood does not exceed 51 μmol / l, the hourly gain of bilirubin - up to 4-5 μmol / L, the liver and spleen moderate increase - 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 cord blood exceeds 68 μmol / l, hourly increment of bilirubin - up to 6-10 μmol / l, liver enlargement - up to 2.5-3.0 cm and spleen up to 1.0-1.5 cm;
• severe: diagnosed by ultrasound of the placenta, indicators of the optical density of bilirubin amniotic fluid obtained with amniocentesis, the amount of hemoglobin and the value of hematocrit blood obtained during cordocentesis. If untimely started or inadequate treatment, icteric form may be accompanied by the development of the following complications.

Nuclear jaundice

In this case, there are signs that indicate a lesion of the nervous system. First, in the form of bilirubin intoxication (lethargy, pathological yawning, loss of appetite, regurgitation, muscle hypotension, disappearance of the second phase of the Moro reflex), and then bilirubin encephalopathy (forced position of the body with opisthotonus, brain cry, bulging of the fontanelle, disappearance of the Moro reflex , seizures, pathological oculomotor symptoms - a symptom of the "setting sun", nystagmus, etc.).

Biliary congestion syndrome, when jaundice acquires a greenish tinge, the liver somewhat increases in comparison with the previous days, a tendency to achioli appears, the saturation of urine color increases.

Anemic form of hemolytic disease of newborns

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

Along with changes in the fetal body, there are changes in the placenta. This is expressed in an increase in its mass. If the norm of the ratio of the mass of the placenta to the mass of the fetus is 1: 6, then in the case of Rh-conflict - 1: 3. The increase in the placenta occurs mainly due to its edema.

But this is not limited to the pathology of Rh-conflict. In addition to the above, with Rh-conflict, antenatal (pre-natal) fetal death and repeated spontaneous abortions are noted.

And with high activity of antibodies spontaneous abortions can occur in the early stages of pregnancy.

In women who have suffered Rh-conflict, most often develop toxicosis of pregnancy, anemia, impaired liver function.

[6], [7], [8], [9], [10], [11], [12], [13]

Classification

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

• if the erythrocytes of the mother and fetus are incompatible in Rh-factor;
• if incompatible with the ABO system (group incompatibility);
• if incompatible with rare blood factors.

The clinical manifestations are:

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

By severity, the icteric form is classified as light, of medium severity and severe.

In addition, distinguish complicated (nuclear jaundice, bile condensation syndrome, hemorrhagic syndrome, kidney damage, adrenal gland, etc.) and uncomplicated form of hemolytic disease of the newborn.

[14], [15]

Diagnosis of hemolytic disease of newborns

Diagnosis of hemolytic disease of newborns is based on immunological examination of the pregnant, ultrasound, dopplerometry of the placenta and utero-placental blood flow, electrophysiological methods of examination, amniotic fluid studies (during amniocentesis), cordocentesis and fetal blood test.

Immunological study allows to determine the presence of antibodies, as well as the change in their number (increase or decrease in the titer). Ultrasound can measure the volume of the placenta, determine the increase in its thickness, detect polyhydramnios, increase the size of the liver and spleen of the fetus, increase the size of the abdomen of the fetus compared with the size of the head and chest, ascites in the fetus. Doppler can detect an increase in systolic-diastolic ratio and resistance index in the artery of the umbilical cord and an increase in the rate of blood flow in the middle cerebral artery of the fetus. Electrophysiological methods (cardiotocography with determination of the index of the fetal condition) allow to detect a monotonous rhythm with moderate and severe forms of the disease and a "sinusoidal" rhythm in the edematous form of GBP. The study of amniotic fluid (during amniocentesis) allows to determine the increase in the optical density of bilirubin in amniotic fluid. Finally, cordocentesis and fetal blood test can detect a decrease in hematocrit, a decrease in hemoglobin, an increase in the concentration of bilirubin, an indirect Coombs test and determine the blood type of the fetus, the presence of Rh factor.

Since the prognosis for the disease depends on the bilirubin content, the birth of a child with suspected hemolytic disease of the newborn for the development of further medical tactics should first of all make a biochemical blood test with the determination of the concentration of bilirubin (total, indirect, direct), protein, albumin, ACT, ALT, and then conduct a survey to determine the etiology of hyperbilirubinemia. For this purpose, the newborn is given a general blood test, rhesus-affiliation is determined for possible Rh-sensitization and blood group with possible ABO-sensitization, the antibody titer is determined and the Coombs direct reaction is performed.

[16], [17], [18]

Differential diagnostics

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

• violation of the morphology of erythrocytes (microspherocytosis, ellipotocytosis, dentocytosis);
• 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 an anamnesis about the presence in the family of other carriers of this pathology and carry out the following studies:

• definition of the morphology of erythrocytes;
• Determination of osmotic resistance and erythrocyte diameter;
• determination of the activity of erythrocyte enzymes;
• determination of the type of hemoglobin.

[19], [20], [21], [22], [23], [24]

Treatment of hemolytic disease of newborns

First of all, if we are talking about Rh-conflict, it is necessary to diagnose the disease during fetal development, to assess its severity and, accordingly, the prognosis of the disease and to treat before the fruitfulness of the viability. All the therapeutic and prophylactic methods used in this period of the fetus's life are divided into non-invasive and invasive methods.

Non-Invasive Methods

Non-invasive methods include plasmapheresis and the introduction of a pregnant intravenous immunoglobulin.

Plasmapheresis of the pregnant woman is carried out with the purpose of detoxification, reocorrection and immunocorrection.

Contraindications to plasmapheresis:

• severe cardiovascular damage;
• anemia (hemoglobin less than 100 g / l);
• hypoproteinemia (less than 55 g / l);
• hypocoagulation;
• immunodeficiency status;
• allergic reactions in the anamnesis on protein and colloid preparations, anticoagulants.

Immunoglobulin for intravenous administration is used to inhibit the production of native maternal antibodies and blockade of Rh-linked antibodies in their placental transport. Use immunoglobulin for intravenous administration at a dose of 0.4 g per kilogram of body weight of the pregnant woman. This dose is distributed for 4-5 days. Repeat the introduction course every 3 weeks before delivery. This method of treatment is not considered universally recognized, since in the severe course of the disease the outcome for the fetus improves slightly.

Invasive methods

Invasive methods include cordocentesis and intrauterine transfusion of erythrocyte mass. These procedures are performed only with Rh-sensitization, currently it is the only pathogenetic method of treatment of hemolytic disease of the fetus.

Indication for the cordocentesis:

• burdened obstetric anamnesis (death of previous children from severe forms of hemolytic disease of newborns);
• high antibody titer (1:32 and higher);
• with ultrasound - signs of hemolytic disease of the fetus;
• high values of the optical density of bilirubin in the amniotic fluid obtained in amniocentesis (3rd zone of the Lily scale).

Terms during which the cordocentesis is carried out: from 24th to 35th week of pregnancy.

Indications for intrauterine transfusion of erythrocyte mass when the fetus is positive for the positive factor is reduced hemoglobin and hematocrit more than 15% of the norm, determined at the time of pregnancy. For intrauterine transfusion of erythrocyte mass, only "washed" erythrocytes 0 (1) of the blood group Rh-negative are used. Intrauterine transfusion of erythrocytic mass 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, in the first place, the treatment of hyperbilirubinemia, the second - correction of anemia and, finally, posidrome therapy aimed at restoring the functions of various organs and systems. All newborns with cat's disease are not applied to the chest, but are fed artificially in the first 5-7 days of life, because antibodies can penetrate the breast milk of a woman and are absorbed in the intestines of newborns, which leads to increased hemolysis.

Treatment of hyperbilirubinemia

Treatment of hyperbilirubinemia involves the use of conservative and operative therapy. Begin with conservative treatment, and at critical values, bilirubin is combined with an operative - exchange (exchange) blood transfusion (PEP).

Conservative therapy includes phototherapy (FT) and the use of immunoglobulin for intravenous administration. Infusion therapy, according to the recommendation of the Russian Association of Perinatal Medicine (RASMM), is conducted in cases of inability to adequately weed out the baby. Phenobarbital is currently not used in practice 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 there is an increase in the CNS depression syndrome.

Phototherapy

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

Indications for phototherapy:

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

Principles of phototherapy:

• dose of irradiation - not less than 8 μW / (cm2хнм);
• the distance from the source to the patient specified in the instructions to the device should be observed;
• you should put the child in a carve;
• protect the eyes and the child's sexual organs;
• It is necessary to change the position of the child under FT lamps every 6 hours.

The minimum concentrations of indirect bilirubin (μmol / L), at which phototherapy is shown

Body weight, g	Age
	24 h	48 h	72 h	4-7 days
<1000	51	85	90	90-120
1000-1500	85	120	150	170
1500-2000	100	120	170	190
2000-2500	120	190	220	240
> 2500	130	200	220	250

Phototherapy is carried out in a constant mode with interruptions for feeding the child for 3-5 days. To abolish FT follows with a decrease in the content of indirect bilirubin below 170 micromol / l.

When carrying out phototherapy, various reactions and side effects may occur.

Complications and side effects of phototherapy

Manifestations	The mechanism of development	Events
Syndrome of "tanned skin"	Induction of melanin synthesis	Observation
Syndrome of the "bronze child"	Accumulation of products of photooxidation of direct bilirubin	Cancel FT
Diarrhea	Activation of the secretory function of the intestine	Observation
Lactase insufficiency	Serous lesions of villous epithelium	Observation, if necessary - cancellation of FT
Hemolysis	Damage to circulating erythrocytes as a result of photosensitization	Cancel FT
Skin burns	Excessive lamp emission	Cancel FT
Eksikoz	Increased fluid loss	Increase the volume of fluid taken by the child
Skin rashes	Increased formation and release of histamine in photosensitization	Observation, if necessary - cancellation of FT

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

Use of immunoglobulin

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

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

Possible regimens for the administration of immunoglobulins:

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

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

Infusion therapy

Infusion therapy is carried out in those cases when it is not possible to adequately weed out the child against the background of the phototherapy. The daily volume of fluid injected into a child should be increased by 10-20% (in children with extremely low body weight - by 40%) compared with physiological needs.

When carrying out infusion therapy, you should monitor the body weight of the child, assess diuresis, electrolyte content, blood glucose, hematocrit.

Infusion therapy mainly involves transfusion of 10% glucose solution4. Infusion therapy is performed intravenously or intragastric by the gastric tube. Intragastric fluid administration can be started from the 3rd-4th day of life, 25% magnesium sulfate solution can be added to the dropper to prevent the development of cholestasis in a dropper, 5 ml / kg, but-spawning 0.5 ml / kg, 4% potassium solution chloride - 5 ml / kg. With intragastric fluid administration, there is no need to reduce the volume of feeds.

Operative therapy - replacement blood transfusion

Distinguish early (in the first 2 days of life) and later (from 3 days of life) ZPK.

Indications for late ZPK are values of the concentration of indirect bilirubin, equal to 308-340 μmol / l (for full term neonates).

Indication for late replacement blood transfusion in newborns, depending on body weight at birth

Body weight, g	Concentration of indirect bilirubin, μmol / l
<1500	220 * -275
1500-1999	275 * -300
2000-2499	300 * -340
> 2500	340-375

1 * The minimum values of bilirubin are indications for the beginning of appropriate treatment in cases when pathological factors that increase the risk of bilirubin encephalopathy (anemia, Apgar score at the 5th minute less than 4 points, Pa02 less than 40 mmHg, act on the child's organism). Duration of more than 1 hour, arterial blood pH less than 7.15 for more than 1 hour, rectal temperature less than 35 ° C, albumin concentration less than 25 g / l, worsening neurological status against hyperbilirubinemia, generalized infectious disease or meninge t).

When the first symptoms of bilirubin intoxication appear, immediate ZPK, regardless of bilirubin concentration, is shown.

Selection of drugs for replacement blood transfusion

In isolated Rh conflict, Rhesus negative group blood and blood are used in the blood of the child, but plasma AB (IV) of the blood group can be used. In case of isolated group conflict, the erythrocyte mass of 0 (1) of the group coinciding according to the Rhesus factor with the Rhesus factor of the baby's erythrocytes and the plasma AB (IV) or one group with the child's blood group is used. With the possibility of development and Rh incompatibility, and incompatibility in the ABO system, as well as after intrauterine blood transfusions for PEP, Rhesus-negative erythrocyte mass 0 (1) of the blood group and plasma AB (IV) or one group with the blood group of the child are used.

When hemolytic disease of a newborn with a conflict over rare blood factors, donor blood that does not have a "conflict" factor is used.

Calculation of the volume of drugs for replacement blood transfusions

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

The ratio of erythrocyte mass and plasma depends on the initial concentration of hemoglobin before the beginning of the operation. The total volume consists of the volume of erythrocyte mass necessary for the correction of anemia, and the volume of erythrocyte mass and plasma required to achieve the volume of PID. The volume of erythrocyte mass necessary for the correction of anemia is calculated by the formula:

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

Of the total volume, subtract the volume of erythrocyte mass necessary for the correction of anemia; the remaining volume is replenished with erythrocyte mass and plasma in a ratio of 2: 1. The foregoing corresponds approximately to the following ratio of erythrocyte mass depending on the concentration of hemoglobin in the child.

Erythrocyte mass	Plasma
120 g / l	1
100 g / l	1
80 g / l	1

[25], [26], [27], [28], [29],

The technique of replacement blood transfusion

ZPK conduct through one of the large vessels (umbilical vein, subclavian vein). Before PID, blood is taken to determine the concentration of bilirubin, the compatibility of the donor's blood and the recipient. ZPK is carried out in a "pendulum way", i.e. Deducing and introducing alternately a portion of blood from the calculation to 5-7 ml per kilogram of the baby's weight. Before the onset of PID, plasma can be administered at a rate of 5 ml / kg. Begin ZPK with deducing blood. Before the onset of PTC and on its course, the catheter is washed with a solution of sodium heparin.

At the initial concentration of hemoglobin below 80 g / l, ZPK begins with correction of anemia, i.e. With the introduction of only erythrocyte mass under the control of the hemoglobin content. After reaching a hemoglobin concentration of 160 g / l, the erythrocyte mass and plasma are introduced. To do this, you can dilute the erythrocyte mass with plasma, and you can alternately enter two syringes of erythrocyte mass and one plasma syringe.

At the end of the ZPK, blood sampling is repeated to determine the bilirubin concentration. After ZPK continue conservative therapy.

ZPK can be accompanied by the development of immediate and delayed side effects.

Complications of replacement blood transfusion

Manifestations		Events
Cardiac	Arrhythmia	Control of cardiac activity
	Volumetric overload
	Heart failure
Vascular	T rhomboemboia, air embolism	Compliance with blood transfusion techniques
	Thrombosis	Catheter washing with sodium heparin solution
Coagulation	Overdose of heparin sodium	Control of the dose of sodium heparin
	Thrombocytopenia	Control of the number of platelets
Electrolytic	Hyperkalemia	For prevention for every 100 ml transfused (erythrocyte mass and plasma in total), introduce 1-2 ml of a 10% solution of calcium gluconate
	Hypocalcemia
	Hypernatremia	Control
	Acidosis	Control of CBS
Infectious	Viral	Monitoring donors
	Bacterial	To prevent complications after PID and for the time of finding a catheter in a large vessel, antibacterial therapy is prescribed
Other	Mechanical destruction of donor cells	Control
	Necrotic Enterocolitis	Observation, detection of clinical symptoms, appropriate therapy
	Hypothermia	Control of body temperature, warming
	Hypoglycaemia	For prophylaxis for each transfused 100 ml (erythrocyte mass and plasma in total), enter 2 ml of 10% glucose solution4
The "graft versus host" reaction		Transfuse blood products exposed to radiation
		Do not use large volumes for ZPK

Late anemia develops 2-3 weeks after PID. Usually it is hyporegenerative and hypoerythropoietic in nature. For its correction use recombinant erythropoietin (epoetin alfa subcutaneously 200 IU / kg once every three days 4-6 weeks).

When iron deficiency is detected against the background of recombinant erythropoietin treatment, iron preparations in a dose of 2 mg / kg of ingested iron are included in the therapy.

Prevention

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

To prevent the development of Rh-sensitization of all women who have Rh-negative blood, during the first 72 hours (preferably the first day) after childbirth with Rh-positive blood from a newborn or in case of an abortion, both spontaneous and non-spontaneous, one dose of anti-D-rhesus immunoglobulin.

In order to prevent all the negative consequences of Rhesus conflict and conflict over other blood factors, it is necessary to determine the blood group of the future mother and, if it is found that there is Rh-negative blood, then it should be ascertained whether this woman has transferred Rh-positive blood (and, in general, if any blood was poured); to find out what kind of account the real pregnancy is (was there before artificial or spontaneous abortion, intrauterine fetal death, premature birth or the death of a newborn soon after birth from jaundice). Of great importance is also information about the Rh factor of the father of the unborn child.

For the purpose of prevention, in addition to all the above, apply antiresus - immunoglobulin. This is done either after the birth of a Rh-positive child, or after the first artificial abortion. It is administered intramuscularly, once, no later than 72 hours after delivery. This specific prophylaxis of Rh-conflict is possible only in non-sensitized women (sensitization - sensitization), that is, in those who have not been transfused with Rh-positive blood, they did not have abortions or miscarriages, and in general, this pregnancy is the first.

In addition to specific prevention, nonspecific is also carried out. It includes various medications that reduce the sensitization of the body and increase its immunobiological protective forces. Sometimes, for the same purpose, use of a pregnant skin flap of the husband is used.

Forecast

In the edematous form of GBPiN, the prognosis is least favorable, which is due to the severity of the child's condition at birth. In icteric form, the prognosis depends on the extent of the CNS lesion, the severity of bilirubin encephalopathy. With anemic form, the forecast is most favorable.

Perinatal mortality in GBPiN is 2.5%. Psychic and psychomotor development of children who have transferred such a condition as hemolytic disease of newborns, in the overwhelming majority corresponds to age norms. 4.9% of children report a backlog in physical development. The pathology of the central nervous system is found in about 8% of children.

[30], [31], [32], [33], [34], [35]