Anemia is characterized by a decrease in the number of red blood cells, hematocrit, or hemoglobin concentration> 2 SD below the mean of a certain age. Anemia in infants may be caused by an increase in the number of red blood cells lost or the production of inadequate red blood cells. This case is unique enough to discuss.
The development of the hematopoietic system must be understood to evaluate infants with anemia. Erythropoiesis begins in the yolk sac at 2 weeks of gestation, producing cells that suppress embryonic hemoglobin. At 6 weeks gestation, the liver is the main site of RBC production, and the cells produced suppress fetal hemoglobin. After 6 months of gestation, the bone marrow becomes the main site for hematopoiesis. During fetal life, erythrocytes experience a decrease in size and an increase in number: the hematocrit increases from 30% -40% during the second trimester to 50% -63%. In late pregnancy and postpartum, red blood cells gradually switch from fetal hemoglobin production to adult hemoglobin production.
After the baby is born, red blood cell mass usually decreases along with increased oxygen and decreased erythropoietin. Red blood cells decrease until the body is deprived of oxygen for metabolism and erythropoietin production is stimulated again. In normal infants, the low point of red blood cells, a physiological response in postnatal life, is not a haematological 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 have decreased hemoglobin concentrations after birth, with a decrease that is usually more sudden and more serious than those of normal-born babies. The hemoglobin level of preterm infants is 7- 9 g / dL at 3-6 weeks of age. Anemia due to prematurity is triggered by lower hemoglobin levels at birth, decreased red cell lifespan, and a suboptimal erythropoietin response. Anemia of prematurity can be exacerbated by physiological factors, including frequent blood sampling and possibly significant clinical accompanying symptoms.
Blood loss, a common cause of anemia in the neonatal period, can be acute or chronic. This condition can be caused by cord abnormalities, placenta previa, placental abruption, traumatic delivery, or bleeding in the baby. As many as 1½ of all pregnancies, fetal-maternal bleeding can be demonstrated by identifying fetal cells in the mother's circulation. Blood can also be transfused from one fetus to another in monochorionic twin pregnancies. In some pregnancies, this condition can get worse.
The rapid destruction of red blood cells may be triggered by the immune or non-immune systems. Isoimmune hemolytic anemia is caused by ABO, Rh, or small groups of blood mismatch between mother and fetus. Maternal immunoglobulin G antibodies and fetal antigens can connect via the placenta and enter the fetal bloodstream, causing hemolysis. This disorder has a broad clinical impact, ranging from mild, limited, to lethal. Because the mother's antibodies take several months to recover, babies who are already infected will experience prolonged hemolysis.
ABO incompatibility usually occurs when a type O mother carries a type A or B fetus. Because A and B antigens circulate widely in the body, ABO incompatibility is usually less severe than Rh disease and is not affected by delivery. In contrast, hemolytic Rh disease rarely occurs during the first pregnancy because sensitization is usually caused by exposure of the mother to RH-positive fetal cells prior to delivery. With the widespread use of Rh immunoglobulins, cases of Rh incompatibility are now rare.
Abnormalities in red blood cell structure, enzyme activity, or hemoglobin production can also cause hemolytic anemia because the abnormal cells are removed faster from the circulation. Hereditary spherocytosis is a disorder caused by defects in the cytoskeletal protein so that its shape becomes brittle and inflexible. Glucose-6-phosphate dehydrogenase deficiency, an X-linked enzyme disorder, usually causes episodic hemolytic anemia that occurs in response to infection or oxidant stress. Thalassemia is an inherited disorder caused by defective hemoglobin synthesis and is 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 sickle characteristics may not necessarily have the disease, whereas children who have sickle cell disease may have hemolytic anemia which is associated with various clinical effects. The symptoms of sickle cell anemia are characterized by a decrease in the amount of fetal hemoglobin and an abnormal increase in hemoglobin S, usually appearing after the child is 4 months old.
Infants and children may have serious bacterial infections, dactylitis, liver or spleen disorders, aplastic crises, vasocclusive crises, acute chest syndrome, priapism, stroke, and other complications. Other hemoglobinopathies include hemoglobin E, the most common hemoglobinopathy worldwide. Hemolytic anemia can also be caused by infection, hemangioma, vitamin E deficiency, and disseminated intravascular coagulation.
Impaired red blood cell production may be an inherited condition. Diamond-Blackfan anemia is a rare congenital macrocytic anemia in which the bone marrow exhibits some erythroid precursors, although the blood cell and platelet counts are generally normal or slightly elevated. Fanconi anemia is a congenital syndrome of bone marrow failure, although it is rarely detected as a child. Other congenital anemias include congenital dyserythropoietic anemia and sideroblastic anemia.
Iron deficiency is a common cause of microcytic anemia in infants and children, and usually peaks when the child is 12-24 months. Premature babies have less iron stores so they are prone to early deficiency. Babies who lose iron due to frequent laboratory sampling, surgical procedures, bleeding, or anatomical abnormalities also cause the baby to become iron deficient more quickly. Blood loss in the intestines 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 contain sufficient folic acid, deficiency of this vitamin 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 babies 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. Malabsorptive syndromes, necrotizing enterocolitis, and other intestinal disorders, such as certain medications or congenital disorders, can put babies at high risk.
Other disorders of red blood cell production may be triggered by chronic disease, infection, malignancy, or transient, transient, and normochromic anemia as a result of viral damage to the precursor erythroids. Although babies can develop the above disorders, most cases occur at the age of 2-3 years.
Examination for anemia in infants should include a medical history and physical examination, cardiovascular status, jaundice, organomegaly and physical anomalies. Initial laboratory evaluation should include a complete blood count with a red cell index, reticulocyte count, and a 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 the anemia and the underlying disease. Transfusions may be required to restore oxygen to the tissues. Certain clinical conditions may require exchange transfusion .
Comment: Premature babies are at risk of iron deficiency because they do not benefit from the full third trimester of pregnancy, during which babies born normally get enough iron from the mother (unless the mother is very iron deficient) to spare until the baby weighs twice the birth weight. In contrast to premature babies, normal babies (except for those with bleeding) are not at high risk of developing iron deficiency anemia in the first months.
When the body runs out of iron stores, 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 an oxygen carrier. Mitochondrial electron transport, neurotransmitter function, and detoxification, as well as catecholamines, nucleic acids, and lipid metabolism are all dependent on iron. Lack of iron causes systemic disturbances that have long-term consequences, especially during the developing child's brain.
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