Hemolytic disease of the newborn

Hemolytic disease of the newborn (synonym erythroblasts fetus) is a severe disease characterized by enhanced dissolution of red blood cells (hemolysis) and the number of symptoms (edema, jaundice, anemia), associated with the toxicity of the products of hemolysis on the body. In the basis of the disease is an incompatibility between the blood of the mother and fetus, more often on RH factor (see). Hemolytic disease of the newborn occurs and when the incompatibility of the blood of the mother and foetus blood group (see), as well as other, less studied factors.
RH factor is contained in red blood cells 85% of people called the RH-positive, the other is called rhesus negative. RH factor is inherited, so if you have it at least one of the parents, it can be passed on to the baby.
If an RH-negative woman pregnant RH-positive fetus (in the case of inheritance from a rhesus-positive father), then going RH-antigen through the placental barrier in the mother's body formed RH antibodies. Last, penetrating into the blood of the fetus, leading to hemolytic processes. The impact of the decay products of hemoglobin (mainly indirect bilirubin) at various organs of the fetus and hematopoietic system causes hemolytic disease of the newborn. Predisposing factors: violation of the permeability of the placenta, lack of enzymatic activity of liver newborn in the translation process indirect bilirubin direct, state of hypersensitivity rhesus negative women to RH factor, repeated pregnancy and blood transfusion woman excluding rhesus factor, sensitizing health and other Value of these predisposing factors confirmed by the fact that hemolytic disease of the newborn is developing in one case from 20-25 RH conflict. In early manifestation (on 5-6th month. pregnancy) rhesus incompatibility may be the cause of premature delivery, miscarriage, fetal death of the fetus. Hemolytic disease of the newborn is manifested in edematous, jaundice and anemia forms.
Total congenital swelling is one of the most severe manifestations of hemolytic disease of the newborn, developing fetus during the period of intrauterine development. This form is more often in children between 5-7th of pregnancy. Children are born pale, with severe swelling of subcutaneous tissue, the presence of fluid in the cavities, with an enlarged liver and spleen. Jaundice is missing, because due to the high permeability of the placenta bilirubin passes into the mother's body and removed from jelchew. In the blood of many young forms of erythrocytes (erythroblastes, normoblastov, reticulocytes). Often children are stillborn or die within the first hours after birth.
When icteric form the main feature is the yellowish color of skin of the child in the coming two days after delivery. Simultaneously marked increase in liver, spleen, anemia, presence of young forms of red blood cells (erythroblastes, normoblastov, reticulocytes). The intensity of jaundice is growing in the next 2-3 days, skin color takes different shades - from lemon yellow to saffron. Jaundice is enhanced parallel to the increase in blood levels of indirect bilirubin, sometimes reaching 30 mg%, hourly buildup of bilirubin may be of 0.4 - 0.9 mg% (in norm - from 0.01 to 0.19 mg%).
The General condition of the child is determined by the intensity of bilirubin toxicity and Central nervous system. In the first days after birth the child is lethargic, bad sucks, there are frequent regurgitation, vomiting. Increased levels of bilirubin up to critical concentration (18 - 20 mg% for full-term and 15 mg% for premature babies) leads to the fact that it penetrates the blood-brain barrier, affecting brain cells. The Central nervous system (the so-called kernicterus, or bilirubin encephalopathy) in a child with hemolytic disease of the newborn is expressed by convulsions, oculomotor violations, stiff neck, symptom, "setting sun" (involuntary turn eyeballs down, and therefore between the top edge of the cornea and the upper eyelid visible band sclera). In addition, is the deposition of crystalline bilirubin in cerebral layer kidney - develops bilirubin heart attack. Violation of the liver hemolytic disease of newborns is manifested not only a violation of education direct bilirubin, and reduced the synthesis of protrombina and protein. Load liver products of hemolysis often leads to violation phase excretion with the development of mechanical jaundice - a so-called syndrome thickening of bile. Usually in children with hemolytic disease of the newborn stool bright yellow color. When "syndrome thickening bile" discolored feces, liver further increases in the blood increases the level of direct bilirubin in the urine lot of bile pigments.
Forecast when icteric form of hemolytic disease of the newborn depends on the extent of involvement of the Central nervous system. When the indirect bilirubin level below the critical forecast for life and development of the child favorable. In case of severe intoxication and development of nuclear jaundice, if the child does not die on the 5-7th day of life from paralysis of the respiratory centre, in the future, there is retarded mental and physical development.
Anemic form of hemolytic disease of the newborn is manifested mainly changes in the blood (anemia, erythroblasts). The forecast in this case more favorable.
Hemolytic disease of the newborn caused by incompatibility between the blood of the mother and fetus, is less common than caused by incompatibility on RH factor. This is because the placenta less permeable for alpha - and beta - agglutinins. Pathogenesis similar RH conflict with the only difference that in this case as antigen are the a and b antigens of red blood cells of the fetus, and the mother's immune α - or beta-agglutinin (see the blood Group). The course and prognosis hemolytic disease of the newborn incompatibility of blood groups favorable, although in this case can be serious clinical manifestations.
The diagnosis of hemolytic disease of the newborn is based on clinical and laboratory data, such as jaundice (see) in the first two days of a child's life, increased levels of bilirubin, a positive test Kumbsa (see Kumbsa reaction), the presence of antibodies in the mother's blood.

Treatment of hemolytic disease of the newborn should be aimed at stimulating the linking and removal from the body of the child toxic indirect bilirubin, as well as the restoration of the functions of the affected organs and systems. To remove bilirubin newborn in the first two days after birth is a replacement transfusion. While intravenous 600-800 ml donor rhesus negative blood and at the same time take 500-700 ml of blood of the child. After replacement transfusion carry out a fractional intravenous infusion of blood, plasma, plazmozameshchath solutions (penistone, neocompsa), appoint excessive drinking or drip subcutaneous and intravenous infusion 5% solution of glucose, ringer's solution. It is necessary to widely apply the b vitamins (B1, B2, B6, B12). The feeding of a child in mother's milk is allowed only after 20-22-day life when almost in milk disappear RH antibodies. Up to this point feeding spend donor or boiled breast milk. Treatment of late complications hemolytic disease of the newborn (the Central nervous system, late anemia) have given the nature of these complications.