Every person has a specific blood group: A (second), B (third), AB (fourth), or zero (0 – first). The letters are used to refer to various antigens that are contained in the blood of a particular person. In addition to these antigens, in the blood of 85% of people there are so-called Rh antigens or Rh factor. There are several types of Rh antigens. They are denoted by the letters D, E and C or the symbols Rh o, Rh ’, Rh”. If the blood does not contain Rh antigen, then the talk is about the Rh negative factor. In the presence of Rh-antigen, blood is considered Rh-positive. How is it connected with hemolytic disease of the newborn? Read on to find out.
Hemolytic Disease of the Newborn
Hemolytic disease of the newborn is a disease that is caused by the incompatibility of the blood of the mother and the fetus in various antigens. More often it develops with incompatibility on the Rh factor: if the mother is Rh-negative and the fetus is Rh-positive. With group incompatibility, the mother often has blood group 0 (I), and the fetus has another one. But it is very rare that hemolytic disease of the newborn can develop if there is a mismatch of other blood antigens (except for the group and the Rh factor).
Hemolytic disease in Rhesus conflict is a serious and dangerous disease, occurring in 99% of women with negative Rhesus. The process of the disease is very simple: during pregnancy, Rh antigens penetrate through the placenta from the fetus to the mother. In response to this “invasion”, maternal blood “produces” Rh antibodies for destroying the Rh-positive red blood cells of the fetus, damaging its liver and spleen, blood-forming organs, and bone marrow. The destruction of red blood cells leads to the accumulation of bilirubin in fetal tissues, which is very toxic to the brain of the fetus and newborn.
The Rh factor in the baby’s blood is established from the third month of intrauterine development. Consequently, from now on, Rhesus antigens begin to enter the maternal organism.
Increased antibody concentration (sensitization) against blood antigens in the body of a Rh-negative woman is possible after transfusion of incompatible blood (conducted even in early childhood), during previous pregnancies and childbirth (if the fetus had Rh-positive blood), after abortions, miscarriages, surgeries for ectopic pregnancy.
In the case of Rhesus conflict, a healthy baby with physiological jaundice can be born. The cause of its occurrence is in the immaturity of liver enzymes, which are activated in premature babies only by the second – third week after birth. Then there is a “self-destruction” of this type of disease. As a rule, physiological jaundice does not adversely affect the child: there is no increase in the liver and spleen, there is no anemia.
Classification of Hemolytic Disease of the Newborn
- Edematous form;
- Icteric form;
- Anemic form.
- Anemic form is the mildest one. From clinical manifestations only insignificant pallor is noted, the increased fatigue of the child is also possible.
- With the icteric form, the child is born with icteric skin, the jaundice rises rapidly and can last up to 3-4 weeks, the child is pale, sluggish, the appetite is reduced, during feeding the baby gets tired quickly, neurological disorders in the form of convulsions and a frozen look can also take place.
- Edematous form is the most severe. Children are often born prematurely, stillbirth is often noted, newborns are edematous. Wax-like skin, icteric staining is pronounced, cyanotic skin is possible. In the pleural cavity and in the abdominal cavity there is a large amount of fluid. Hemophilia is dramatically increased.
The development of hemolytic disease is not always determined by the concentration of isoimmune antibodies of the mother. The degree of maturity of the body of the newborn matters as well: the disease is more severe in premature babies.
Hemolytic disease of newborns with incompatibility in the ABO system proceeds somewhat more easily than during rhesus conflict. But with maternal diseases during pregnancy, an increase in the permeability of the placental barrier occurs and then the formation of more severe forms of hemolytic disease is possible.
The diagnosis is based on the history (anamnesis) of life and the current pregnancy of the mother and the clinical symptoms of the child, the determination of the blood group and the mother’s and the baby’s rhesus, the baby’s blood test, the determination of the bilirubin level, the rhesus antibody titer and specific immunological factors in the blood and mother’s milk. For the purpose of antenatal (prenatal) diagnosis, the level of bilirubin in the amniotic fluid and the concentration of Rh antibodies are determined.
The differential diagnosis is carried out with hereditary hemolytic jaundice, hemorrhage, jaundice with sepsis, cytomegalovirus infection, toxoplasmosis.
Treatment of Hemolytic Disease of the Newborn
The treatment of hemolytic disease of the newborn is complex and is aimed primarily at the rapid removal of toxic erythrocyte decomposition products (hemolysis), bilirubin and antibodies from the body of the newborn, so that the process of hemolysis does not continue after birth. Detoxification solutions, vitamins, ATP, glucose are administered intravenously. Phenobarbital is prescribed, which contributes to the binding and removal of bilirubin. Enterosorbents are also used. Phototherapy is performed with blue lamps. The child must drink plenty of fluids. Vitamins of group B (B1, B2, B6, B12) are also prescribed. With the ineffectiveness of detoxification therapy and with a very rapid increase in the content of bilirubin in the blood, with a marked decrease in the level of hemoglobin, the question of carrying out a replacement transfusion is decided.
It is allowed to apply children to the breast only after the 12-22nd day of life, when the antibodies to the Rh factor disappear in the mother’s milk. Up to this point, feeding is carried out with donor breast milk. Treatment of late complications of hemolytic disease (lesions of the central nervous system, anemia) is carried out according to their severity.
The course and prognosis of the disease depend on its form. With early and adequate therapy, with mild and moderate forms of hemolytic disease, children tend to grow and develop well. When the level of bilirubin is 257-342 μmol / l and more, even if nuclear jaundice has not developed, almost one-third of children may have deviations in their neuropsychological status. Anemia may persist for several months. Children with residual dysfunction of the central nervous system need long-term restorative treatment under the supervision of a neurologist, ophthalmologist and pediatrician.
Preventative measures include determination of blood group and Rh factor in a pregnant woman. Women with Rh negative blood are put on record at the antenatal clinic. At the same time, doctors find out whether a woman has had any blood transfusions, if children have been born with this disease, they detect stillbirths and abortions. If an abortion is made during the first pregnancy or a spontaneous miscarriage occurs, no later than 72 hours (two or three days) an injection of anti-Rh immunoglobulin should be given.
Blood tests for Rh antibodies are regularly carried out, and with their rapid increase in the blood of pregnant women, women are prescribed treatment with anti-D-globulin (anti-rhesus).
Pregnant women with Rh-negative blood are hospitalized and, two to three weeks before the expected date of birth, artificial stimulation of labor is performed, since after the 36th week, the transfer of antibodies from mother to fetus through the placenta is activated. This method is desirable to prevent the formation of severe hemolytic disease of the newborn.