Contents:
Medical Video: Anemia symptoms and treatments - Signs of being anemic
Anemia is characterized by a decrease in the number of red blood cells, hematocrit, or hemoglobin concentration> 2 elementary schools below a certain average age. Anemia in infants may be caused by an increase in the number of missing erythrocytes or inadequate production of red blood cells. This case is quite unique to discuss.
Development of a hematopoietic system must be understood to evaluate infants with anemia. Erythropoiesis starts in the yolk sac at 2 weeks' gestation, producing cells that suppress embryonic hemoglobin. At 6 weeks' gestation, the liver becomes the main place for RBC production, and the cells produced suppress fetal hemoglobin. After 6 months of gestation, the bone marrow becomes the main place for hematopoiesis. Throughout the life of the fetus, erythrocytes decrease in size and increase in number: increased hematocrit from 30% -40% during the second trimester to 50% -63%. At the end of pregnancy and postpartum, red blood cells gradually switch from the production of fetal hemoglobin to the production of adult hemoglobin.
After the baby is born, the mass of red blood cells usually shrinks along with an increase in oxygen and a decrease in erythropoietin. Red blood cells decrease until the body lacks oxygen for metabolism and the production of erythropoietin is stimulated again. In normal infants, the low point of red blood cells, the physiological response to postnatal life, is not a hematological disorder. Usually this condition occurs when the baby is 8-12 weeks old and the baby's hemoglobin level is around 9-11 g / dL.
Premature babies also experience a decrease in hemoglobin concentration after birth, with a decrease that is usually more sudden and more serious than a normal-born baby. The hemoglobin level of a premature baby is 7- 9 g / dL at 3-6 weeks of age. Anemia due to prematurity is triggered by lower hemoglobin levels at birth, decreased age of red blood cells, and suboptimal erythropoietin responses. Anemia of prematurity can be aggravated by physiological factors, including blood sampling too often and the possibility of significant clinical symptoms that accompany it.
Blood loss, a common cause of anemia in the neonatal period, can be acute or chronic. This condition can be caused by abnormalities of the umbilical cord, placenta previa, placental abruption, traumatic labor, or bleeding in the baby. As many as 1½ of all pregnancies, fetal-maternal bleeding can be demonstrated through identification of fetal cells in the mother's blood circulation. Blood can also be transfused from one fetus to another in monocorionic twin pregnancies. In some pregnancies, this condition can be more severe.
The rapid destruction of red blood cells may be triggered by the immune system or non-immune. Isoimmune hemolytic anemia is caused by ABO, Rh, or a small group of blood that does not match between mother and fetus. Maternal immunoglobulin G antibodies and fetal antigens can be connected through the placenta and into fetal blood flow, causing hemolysis. This disorder has a broad clinical impact, ranging from mild, limited, to deadly. Because maternal antibodies take several months to recover, babies who are already infected will experience prolonged hemolysis.
ABO incompatibility usually occurs when type O mothers carry a type A or B fetus. Because A and B antigens are widely circulated in the body, ABO incompatibility is usually not as severe as Rh disease and is not affected by labor. Conversely, Rh hemolytic disease rarely occurs during the first pregnancy because sensitization is usually caused by exposure of the mother to RH-positive fetal cells before labor. With the widespread use of Rh immunoglobulin, cases of Rh incompatibility are now rare.
Abnormalities in red blood cell structure, enzyme activity, or hemoglobin production can also cause hemolytic anemia because abnormal cells are released faster than circulation. Hereditary spherocytosis is a disorder, caused by a defect in the cytoskeletal protein so that its shape becomes brittle and inflexible. The glucose-6-phosphate dehydrogenase deficiency, a disorder of X-linked enzymes, usually causes episodic hemolytic anemia that occurs in response to infection or oxidant pressure. Thalassemia is a hereditary disorder caused by defects in hemoglobin synthesis and classified as alpha or beta according to the infected globin chain. The severity depends on the type of thalassemia, the number of infected genes, the amount of globin production, and the ratio of alpha and beta-globin produced.
Sickle cell anemia is another disorder of hemoglobin production. Children born with crescent characteristics are not necessarily affected by this disease, while children who have sickle cell disease may experience hemolytic anemia associated with various clinical effects. Symptoms of sickle cell anemia are characterized by a decrease in the amount of fetal hemoglobin and an abnormal increase in hemoglobin S, usually after a 4-month-old child.
Infants and children may experience serious bacterial infections, daktilitis, liver or spleen disorders, aplastic crises, vaso-occlusive crises, acute chest syndrome, priapism, strokes, and other complications. Other hemoglobinopathies include hemoglobin E, hemoglobinopathy which is the most common in the whole world. Hemolytic anemia can also be caused by infection, hemangioma, vitamin E deficiency, and disseminated intravascular coagulation.
Disorders of red blood cell production may be a congenital condition. Diamond-Blackfan anemia is a rare inherited macrocytic anemia in which the bone marrow shows several erythroid precursors, although the number of blood cells and platelets is generally normal or slightly increased. Fanconi anemia is a congenital syndrome of bone marrow failure, although it is rarely detected as a child. Other congenital anemia includes congenital dyserythropoietic anemia and sideroblastic anemia.
Iron deficiency is a common cause of microcytic anemia in infants and children, and is usually at its peak when children are 12-24 months old. Premature babies have less iron reserves so they are prone to early deficiency. Iron-deficient babies due to frequent laboratory sampling, surgical procedures, bleeding, or anatomical abnormalities, also cause babies to become iron deficient faster. Blood loss in the intestine caused by consumption of cow's milk can also put the baby at a higher risk. Lead poisoning can be a cause of microcytic anemia, similar to iron deficiency anemia.
Lack of vitamin B12 and folate can cause macrocytic anemia. Because breast milk, pasteurized cow's milk, and infant formula milk contain enough folic acid, this vitamin deficiency is rare in the United States. According to records, goat's milk is not an ideal source of folate. Although rare, vitamin B12 deficiency can occur in infants who drink breast milk from mothers with low B12 reserves. This is caused by the mother who follows a strict vegetable and fruit diet or has pernicious anemia. Malabdominal syndromes, necrotizing enterocolitis, and other intestinal disorders such as certain drugs or congenital abnormalities, can put babies at high risk.
Other disorders of red blood cell production may be triggered by chronic disease, infection, malignancy, or erythroblastopenia, transients, and normochromic anemia as a result of erythroid precursor damage by viruses. Although babies can contract the above disorders, most cases occur at the age of 2-3 years.
Anemia examination in infants must include a medical history and physical examination, cardiovascular status, jaundice, organomegaly, and physical anomalies. Initial laboratory evaluation must include complete blood count with red blood cell index, reticulocyte count, and direct antiglobulin test (Coombs' test). The results of the examination can help determine additional tests. The type of treatment depends on the clinical severity of anemia and the underlying disease. Transfusion may be needed to restore oxygen intake to the tissue. Certain clinical conditions may be needed exchange transfusion.
Comment: Premature babies are at risk of iron deficiency because they do not benefit from the third trimester of full pregnancy, where babies born normally get enough iron from the mother (unless the mother is very iron deficient) as a reserve until the baby's weight is twice the weight at birth . In contrast to premature babies, normal infants (except those who experience bleeding) are not at high risk of developing iron deficiency anemia in the first months.
When the body runs out of iron reserves, the consequences will be more severe than anemia. Iron is a substance that is very important in physiological functions, beyond the role of hemoglobin as a carrier of oxygen. Transport of electron mitochondria, neurotransmitter function, and detoxification, as well as catecholamines, nucleic acids, and lipid metabolism all depend on iron. Iron deficiency causes systemic disorders that have long-term consequences, especially during the growth of the child's brain.
