CLINICAL AND MORPHOLOGICAL PROPERTIES OF HEMOLYTIC DISEASE OF NEWBORNS

Аннотация

Hemolytic disease of newborns (GBN) is a pathological condition that occurs due to an immunological conflict between fetal red blood cells and maternal antibodies. The disease is caused by incompatibility in the antigens of the Rhesus (Rh) system or the ABO blood group system. As a result, red blood cells are destroyed (hemolysis), which leads to anemia, hyperbilirubinemia and various complications. Hemolytic disease of the fetus and newborn (GBN) is an isoimmune hemolytic anemia that occurs due to incompatibility of maternal and fetal blood with erythrocyte antigens, while antigens are localized on fetal erythrocytes, and antibodies to them are produced in the mother's body. Keywords: hemolytic disease of newborns, Rh conflict, ABO incompatibility, anemia, hyperbilirubinemia, bilirubin encephalopathy, jaundice, fetal dropsy, phototherapy, replacement blood transfusion, erythrocyte antigens, Coombs test, antiresus immunoglobulin, hepatosplenomegaly, erythroblastosis. КЛИНИКО-МОРФОЛОГИЧЕСКИЕ ОСОБЕННОСТИ ГЕМОЛИТИЧЕСКОЙ БОЛЕЗНИ НОВОРОЖДЕННЫХ Аннотация. Гемолитическая болезнь новорожденных (ГБН) — патологическое состояние, возникающее вследствие иммунологического конфликта между эритроцитами плода и материнскими антителами. Заболевание обусловлено несовместимостью по антигенам системы резус (Rh) или системы групп крови AB0. В результате происходит разрушение эритроцитов (гемолиз), что приводит к анемии, гипербилирубинемии и различным осложнениям. Гемолитическая болезнь плода и новорожденного (ГБН) — изоиммунная гемолитическая анемия, возникающая вследствие несовместимости крови матери и плода с антигенами эритроцитов, при этом антигены локализуются на эритроцитах плода, а антитела к ним вырабатываются в организме матери. Ключевые слова: гемолитическая болезнь новорожденных, резус-конфликт, несовместимость по системе АВО, анемия, гипербилирубинемия, билирубиновая энцефалопатия, желтуха, водянка плода, фототерапия, заместительное переливание крови, эритроцитарные антигены, проба Кумбса, антирезусный иммуноглобулин, гепатоспленомегалия, эритробластоз. 887 ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3 The etiology and pathogenesis of GBN develops in the presence of an immunological conflict between mother and fetus. Main causes: Rhesus conflict: occurs with a Rh-negative mother and a Rh-positive fetus. Maternal antibodies (IgG) cross the placenta and cause the destruction of fetal red blood cells. ABO-incompatibility: occurs when the blood groups of the mother and child are incompatible (most often if the mother has blood type O and the child has A or B). Other antigenic systems (Kell, Duffy, Kidd) can also cause GBN, but are less common. The main pathogenetic mechanisms: Destruction of red blood cells by maternal antibodies. The development of anemia and tissue hypoxia. The release of free bilirubin, which can lead to bilirubin encephalitis (nuclear jaundice). Activation of compensatory mechanisms, such as erythropoiesis in the liver and spleen, leading to hepatosplenomegaly. Clinical forms and symptoms of GBN can manifest in three main forms: 1. Edematous form (the most severe): Generalized edema (dropsy of the fetus). Severe anemia, heart failure. Marked enlargement of the liver and spleen. High mortality without timely treatment. 2. Jaundice: The appearance of jaundice in the first hours after birth. A sharp increase in the level of indirect bilirubin. The risk of bilirubin encephalopathy. Enlargement of the liver and spleen. 3. Anemic form: Moderate anemia without severe jaundice. Mild hepatosplenomegaly. A more favorable current. Morphological changes In GBN, the following pathological changes are observed: Bone marrow: erythroid germ hyperplasia in response to anemia. Liver and spleen: erythroblast proliferation, fibrosis, blood stagnation. The brain (with severe hyperbilirubinemia): bilirubin encephalopathy with bilirubin deposition in the basal ganglia (nuclear jaundice). Heart and lungs: signs of hypoxia, swelling of tissues. Diagnostics 888 ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3 1. Prenatal diagnosis: Determination of blood type and Rh factor of mother and fetus. Determination of the titer of antiresus antibodies. Ultrasound signs of fetal dropsy. Cordocentesis and amniocentesis for fetal blood analysis. 2. Postnatal diagnosis: Clinical signs (jaundice, anemia, hepatosplenomegaly). Laboratory tests: elevated bilirubin, decreased hemoglobin, positive direct Coombs test. Treatment and prevention 1. Conservative therapy: Phototherapy for the destruction of indirect bilirubin. Intravenous administration of immunoglobulin to reduce hemolysis. 2. Replacement blood Transfusion (RPC): It is used for severe anemia and severe hyperbilirubinemia. The goal is to remove antibodies and excess bilirubin. 3. The use of the antidote phenobarbital (to accelerate the metabolism of bilirubin in the liver). 4. Prevention: Administration of antiresus immunoglobulin to Rh-negative mothers after d