Anemia in children

Anemia in children is a frequent disease. It is connected with the age of apparatus blood; functional immaturity it easy vulnerability under the influence of various factors. There are anemia endogenous and exogenous origin. The former include hemolytic anemia. The cause of hemolysis in newborns may be an incompatibility between the blood of the mother and the fetus by RH factor, blood group (see Hemolytic disease of the newborn). Anemia is accompanied by hemolytic crises caused by genetic instability of erythrocytes. This family hemolytic anemia type Minkowski - soffera (see Hemolytic anemia). Rarely occurs in children acute hemolytic anemia of Lederer. Possible cause of the disease - autoimmunization to erythrocytes. Characterized by acute onset, hemorrhagic syndrome, fever, thrombocytopenia, anisocytosis, poikilocytosis, Hyper-bilirubinemia due to the indirect bilirubin. To anemia endogenous origin include anemia, due to abnormalities of the synthesis of hemoglobin (hemoglobinopathy) - thalassemia (see), in which fetal (embryonic) hemoglobin is 90%, and sickle cell anemia, in which there is abnormal type of hemoglobin (the so-called hemoglobin S), chemical composition different from the normal form of hemoglobin. Sickle cell anemia occurs with severe hemolytic crises, with frequent complications such as brain vessels, hemorrhages. Erythrocytes in this form of anemia have a kind of Crescent-shaped.
Children are also aplastic and regeneratory anemiaassociated with primary constitutional failure of the bone marrow.
Among anemia exogenous origin of the most common nutritional anemia. The disease occurs mainly in children of early agereceiving monotonous milk feeding, which is not present in the diet of a number of amino acidsneeded to build a protein part of hemoglobin. The reason hypochromic anemia is the inability of the body to dispose of iron by a violation of the synthesis of hemoglobin. Some significance in the development of nutritional anemia is a deficiency of microelements (copper, cobalt, magnesium)and vitamins of group B, reduction of endogenous iron stores, which comes from an infant to a five-month age.
Clinical manifestations deficiency anemia depend on the severity of the disease. In the mild form a child's diet is not broken, pallor of skin, puffiness of the face, a modest increase in liver and spleen. The hemoglobin content reduced to 50-60%, the number of erythrocytes to 3-4 million, color index of 0.5-0.7. In severe form of the disease is marked lag a child's height and weight, pastos century, stop, sometimes dotted haemorrhage. The liver and spleen enlarged and are 2-3 cm from the edge of a rib arch. The amount of hemoglobin falls to 15-25%, erythrocytes to 2 million, the colour of the indicator varies around the unit. Leukocytic formula approaches that when leukemia (see Leukemia in children). As a rule, severe nutritional anemia combined with symptoms of rickets. With severe deficiency anemia is associated so-called psevdomatematicheskoe anemia of Yaksha - Hayama, which used to be singled out as a separate disease.
To exogenous anemia are also infectious and post-infectious anemia. By their nature, they hypochromic. Any infectious disease can cause anemia, but most often, the development of anemia associated with pyogenic infection. Toxic anemia usually associated with helminthic invasion. Malignant anemia can cause a wide lentets, Ancylostoma duodenum. Analizatze associated with toxic effects on blood forming organs products of vital activity of parasites. Toxic anaemia gipohromnye in nature and often occur with the expressed eosinophilia (see).
Special group of anemia of prematurity - gipomagniemia anemia. The disease develops from the end of the first month of life. The reason - functional failure of the bone marrow premature, predisposing factors, violations of regime, care, nutrition. Anemia of prematurity is distinguished by persistent nature of the flow.
Treatment of anemia determined primarily by the etiology of the disease. However, there are General principles of treatment of anemia, aimed at improving the overall reactivity of the organism and strengthening of regenerative processes. It is necessary to pay attention to a child's diet. It should be sufficient calories, contain a full complex of proteins, fats, carbohydrates and vitamins. In light and moderate anemia calorie should be increased by 10-12%, with heavy - recommended reducing the first time the daily calorie by 20% by limiting fat. In the diet should include first of all products containing iron and vitamins group b (meat, liver, cheese, eggs, apples, strawberries and others). In addition to a balanced diet, it is necessary to strictly perform hygienic requirements for child care. Widely must be used hydrotherapy, massage, gymnastics, air and sun baths.
Sick children should receive a course of vitamin therapy: vitamin B1 and B2 0,001 - 0,002 g, ascorbic acid 0.1-0.2 g, fish oil for children up to 1 year-on-The-2-1 chain. L., 2 years in the 1-2 chain. L., 3-6 years in the dessert spoon, 7 years and older on 1 table. L. 2-3 times a day. Occupies a special place of vitamin B12, as a pathogenetic treatment perniciously anemia. Babies and children first three years of life vitamin B12 is prescribed in doses of 5 mcg per 1 kg of body weight per day, a day intramuscularly. Find wide application iron supplements in the first place, reduced iron, which appoint 0.05-0.1 g infants and 0.15 - 0.2 g in older age orally 3 times a day after meals with hydrochloric acid. Iron preparations are particularly indicated in patients accompanied with a decline in color indicator. With a sharp decrease in the number of red blood cells, you can apply copper sulphate solution in the form of 1% solution of 5 drops 3 times a day alone or in combination with drugs iron. One of such combined drugs is hemocyanin appointed by the inside of 0.1-0.5 g 3 times a day during meals. Good gemostimuliruyuschee effect have intravenous injections of small and medium quantities single-group of blood (20-50 ml of children under three years of age and 80-120 ml in older age).
In aplastic, gipoplasticheskaya and hemolytic anemia shown hormonal drugs (prednisone, dexamethasone and other) on the appointment of a physician.

Anemia in children is quite common and the younger the child, the easier it occurs anemia. This is due to some functional lability hematopoietic apparatus of children; even a minor and short-acting reasons (malnutrition, adverse hygienic conditions of life, light accidental infections etc) easily cause children anemia. Impaired hematopoiesis, especially in children of early age, often tends to acquire the features of embryonic type, predisposition to the emergence of myeloid and lymphoid metaplasia blood-forming tissue. Along with this there is a marked the blood-forming ability of the device to restore normal blood at elimination of the reasons causing A.
Deficiency in children are endogenous and exogenous origin; the former include also A. with unknown etiology.
Children are relatively frequent hemolytic A. if hemolytic disease of the newborn (see). They should be distinguished from other forms of congenital family hemolytic A. associated with a deficiency of red blood cells (hemolytic anemia Minkowski - soffera) and relatively rarely detected in the first days and weeks of life. More often found anemia installed etiology, arising during or after suffering various diseases (malaria, leishmaniasis and other), helminthic invasions, unhygienic living conditions, after loss of blood, and so on, Frequent cause A. in children of early age is also irrational diet - nutritional A. Clinical and haematological features in each case depend on the defects of the diet, the age of the child and its individual characteristics; often there is such anaemia in children 6-18 months, receiving monotonous milk diet and deprived of a variety of complementary foods. There is insufficient evidence to highlight in particular the clinical form A. when feeding goat milk (printing. table, Fig. 10), although it can be considered that under other equal conditions monotonous feeding goat milk sooner and easier causes anemia than feeding with cow's milk.


Fig. 10. Blood anemia on abuse of goat's milk: 1 - lymphocyte; 2 - polychromatophilia erythrocyte; 3 - normoblast butyronitrile; 4 - normoblast polychromatophilia; 5 - poikilitic (erythrocyte) polychromatophilia; 6 - platelets. Pronounced poikilocytosis; anisoles.

Fig. 11
. Blood anemia of Yaksha - Hayama: 1 - butyronitrile megaloblasts; 2 - polychromatophilia erythrocyte; 3 - mieloza neutrophilic; 4 - polychromatophilia normoblast; 5 - stab neutrophil (1st class). Poikilocytosis; anisoles; oligophrenia.

Fig. 12
. Bone marrow with anemia of Yaksha-Hayama: 1 - polychromatophilia normoblast; 2 - microbiologist; 3 - promyelocyte eosinophilic; 4 - metamyelocyte neutrophilic (young neutrophil); 5 - microbiologist; 6 and 7 - metamyelocyte neutrophilic; 8 - neutrophil segmented (2 and 3 class); 9 - promyelocyte neutrophilic.

In the pathogenesis of alimentary A. have is insufficient intake of vitamins, especially vitamin B12 (external factor castle) and B6, insufficient production of the gastric mucosa - gastropatia (internal factor castle), the shift of the acid-alkaline balance in the direction of acidosis, insufficient intake of minerals, particularly iron (iron deficiency character A.), intestinal poisoning, etc.
Nutritional anaemia are of different severity. In milder forms A. General condition of the child violated little. When A. moderate exhibit common pastos, paleness of the skin and visible mucous membranes, reasonable hyperplasia peripheral lymph nodes and tonsils. The amount of hemoglobin decreased up to 50-60% (8-10 g%), the number of erythrocytes - up to 4 million, rarely up to 3 million, color indicator - 0,5-0,6, polychromatophilia, moderate retikulez, sometimes a single normoblast; white blood cells and blood platelets deviations from the norm there. This form of anemia in children of early age has the character of hypochromic, iron deficiency anemia with moderate symptoms of regeneration.
In severe form, called psevdomatematicheskoe anemia of Yaksha-Hayama, the General condition of the child violated significantly, the outer skin pale and waxy skin or yellowish hue; the eyelids and feet slightly swollen; a point, and sometimes more significant bleeding on the face, trunk, and extremities; a positive symptom Konchalovsky - Tiller - Leede; hypotension muscles; belly big, liver and spleen were enlarged; almost always heavy rickets. The amount of hemoglobin decreased up to 15-25% (2,5-4,5 g%), the number of erythrocytes - to 1.5-2 million and below, a color indicator is about one and more; unsophistication, polychromatophilia, retikulez, normoblasts, often bullock, Jolly and ring Kubota. The total number of white blood cells typically increased to 15-20 thousand and more (leikemia form), lymphocytosis, sometimes monocytosis; almost always the shift of neutrophils left to plasmic order has been revealed, promielozitov and even myeloblasts; basophils are usually absent, eosinophils is within norm, sometimes - aneosinophilia (flowering, table, Fig. 11). The reduced number of platelets or within the normal range. Retraction of a blood clot is expressed poorly. Bleeding time increased.
This severe deficiency anemia, there is no reason to allocate in separate nosological unit; it should be seen as a variant of the alimentary A., as a similar clinical picture may arise under the influence of other etiological factors of congenital syphilis, repeated and chronic infections, etc. But in these cases, the leukocyte formula predominate lymphocytes and neutrophils; kilogramme indicates lively eritro - and leikopoaiza (printing. table, Fig. 12). The severity of the clinical picture with nutritional A. depends on the individual characteristics of the child, the functional properties of his blood-forming system, the nature and duration of exposure etiological factor.
In the differential diagnosis of attitude we need to be aware of post-infectious and hemolytic anemia, leukemia.
Alimentary A. if artificial feeding of dry milk mixtures are features of malignancy (lack of vitamin B12); excessive feeding carbohydrates specified clinical picture develops on the background of carbohydrate eating disorders; A. on the soil of Hypo - and avitaminosis predominate in the clinical picture deficiency symptoms of a vitamin.
Treatment consists of the settlement of diet and mode of life of the child, the elimination of the defects of life, have shown the appointment of iron supplements, vitamins, stimulating and restorative effects (massage, gymnastics, exposure to ultraviolet light, hemotherapy and blood transfusion).
Anemia in premature infants. To anemia are particularly prone to premature children, where it occurs at the end of the 1st or at the beginning of the 2-gomesena life, reaches a maximum of 3-4-th months; the amount of hemoglobin decreases to 30 - 40% (5-7 g%), the number of erythrocytes - up to 3-4 million, color indicator is less than one. Random diseases, defects nutrition, care and household promote earlier detection and more severe and prolonged. In the period of rise of clinical symptoms of anemia is gipomagniemii nature, during repair are detected the signs of recovery of erythropoiesis.
A. premature babies difficult normal Antianemic remedies, but with the right care, educating, feeding and often without any treatment she starts to decrease and, as a rule, disappears to 7-8-th months of life.
Pathogenesis A. premature babies not fully fitted; the most important is temporary functional failure of the bone marrow; effect and the reason for the incomplete; predispose to anemia poverty of child organism with iron to the moment of birth and lack of exposure to fresh air.
Prevention is the proper nutrition, early introduction of supplementary feeding and complementary feeding of food rich in complete protein, vitamins and mineral factors, proper care. Drug prevention has had little effect.
Treatment: blood transfusion, medicines iron, copper, preparations of liver, fish IPR, vitamins, protivorahiticescoe and stimulating therapy.
To anemia endogenous origin, and must include a rarely observed benign constitutional A. where the paleness of the exterior of the skin and reduce the content in the peripheral blood hemoglobin and red blood cells is observed from the first weeks of life of children, but otherwise healthy. A. is gipomagniemii nature, defies the conventional medical treatment, reaches its maximum intensity for 3-6-th months and finally goes to 2-3 years without any treatment. Such A. they should be differentiated from congenital gipoplasticheskaya and homolytic anemia.


Aplastic A. without specific cause, acute-paced and rapidly progressing, observed in children is relatively rare; clinical and hematological picture is not very different from that of A. in adults. The disease should be differentiated from pseudoplasticity A. that occur in immunocompromised children under the influence of various long-term operating negative factors (infection, defects and care, frequent blood loss, and so on). When Troubleshooting etiological factors relatively quickly comes cure under the influence of the usual methods of treatment of anemia. We must remember that the "mask" of aplastic anemia is sometimes quite a long time flow acute leukemia. From other blood diseases should be excluded severe A. on the soil infections (sepsis), essential thrombocytopenia and agranulocytosis.
From gipoplasticheskaya and aplastic A. for children-specific syndrome, Fanconi and Blackfan - diamond. Fanconi syndrome, inherited, reveals clearly more often at the age of 4-5 years. In the pattern of blood manifest anemia, thrombocytopenia and leukopenia.
Pancytopenia usually combined with brown spots on the skin, dwarfism, microcephaly, hypoplasia of the genital organs, strabismus and other birth defects.
Especially often observed anomaly large fingers, underdevelopment, lack or other abnormalities of the radial bone; almost always - delay of mental development. The pathogenesis of the disease is not installed; it should be assumed enzymopathy; and indicate to the reduced activity of peroxidase erythroblasts. The prognosis is unfavorable.
Treatment does not give lasting effect; temporary improvement usually by blood transfusion and the appointment of corticosteroids.
Anemia Blackfan-diamond, which is revealed in infants and young children, hypoplasia is celebrated only by erythroid Rostock bone marrow. The pathogenesis is unknown; point to a disorder of the metabolism of tryptophan and the impact of an enlarged thymus.
Forecast serious. Regular RBC transfusions and the appointment of corticosteroid allow a relatively long time to maintain a satisfactory condition of the patient.
Pernicious anemia Addison - Biermer on children as a rule, is not observed; pernitsiosna anemia, one can observe when parasitic infestations (especially a lentetsom), the rapid shutdown of the stomach after severe burns of the esophagus and other major diseases.
From the true form of anemia in children it is necessary to distinguish apparent (imaginary) anemia, where pale skin does not depend on low number of hemoglobin and red blood cells, and on the characteristics of the blood supply and distribution of skin capillaries in children.
These children are not shown Antianemic remedies and restorative effects, proper physical education, physical education, sports, water procedures.
The main factors of treatment of all forms A. in children: elimination of etiological causes, creation of favorable conditions of life and nutrition, appropriate use of effects of natural factors of nature and sports. Therapeutic diet should be rich in complete protein, mineral basis, vitamins, but without excess fat, hypochromic A. shown prescriptions, iron, copper, vitamin B6 and other vitamins; when hyperchromic anemia best effect gives the liver drugs, vitamin B12, drugs cobalt.
Are also transfusion of whole blood and erythrocyte mass. When gipoplasticheskaya A. needed a bone marrow transplant, aplastic and haemolytic anaemia - removal of the spleen. In the treatment of all forms A. shown wide use of methods of stimulating therapy (proteinuria, intramuscular hemotherapy, ultraviolet radiation, and so on). Hemolytic, autoimmune and other heavy A. - corticosteroids.