Mkb 10 international classification of diseases of anemia. Iron deficiency, chronic and hemolytic anemia

ICD 10. Class III. Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism (D50-D89)

Excludes: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine, nutritional and metabolic disorders (E00-E90), human immunodeficiency virus [HIV] disease (B20-B24), injury, poisoning and certain other effects of exposure external causes(S00-T98), neoplasms (C00-D48), symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified (R00-R99)

This class contains the following blocks:

D50-D53 Dietary anemia

D55-D59 Hemolytic anemias

D60-D64 Aplastic and other anemias

D65-D69 Coagulation disorders, purpura and other hemorrhagic conditions

D70-D77 Other diseases of the blood and blood-forming organs

D80-D89 Selected disorders involving the immune mechanism

The following categories are marked with an asterisk:

D77 Other disorders of the blood and blood-forming organs in diseases classified elsewhere

NUTRITIONAL ANEMIA (D50-D53)

D50 Iron deficiency anemia

D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.

Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)

D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson Syndrome

D50.8 Other iron deficiency anemias

D50.9 Iron deficiency anemia, unspecified

D51 Vitamin B12 deficiency anemia

Excludes: vitamin B12 deficiency (E53.8)

D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.

Congenital intrinsic factor deficiency

D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.

Imerslund (-Gresbeck) syndrome. Megaloblastic hereditary anemia

D51.2 Transcobalamin II deficiency

D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Vegetarian anemia

D51.8 Other vitamin B12 deficiency anemias

D51.9 Vitamin B12 deficiency anemia, unspecified

D52 Folate deficiency anemia

D52.0 Dietary folic deficiency anemia. Megaloblastic nutritional anemia

D52.1 Folate deficiency anemia drug-induced. If necessary, identify the drug

use additional external cause code (class XX)

D52.8 Other folate deficiency anemias

D52.9 Folic deficiency anemia, unspecified Anemia due to inadequate intake of folic acid, NOS

D53 Other nutritional anemias

Includes: megaloblastic anemia not responding to vitamin therapy

nom B12 or folates

D53.0 Anemia due to protein deficiency. Anemia due to lack of amino acids.

Excludes: Lesch-Nychen syndrome (E79.1)

D53.1 Other megaloblastic anaemias, not elsewhere classified. Megaloblastic anemia NOS.

Excludes: Di Guglielmo's disease (C94.0)

D53.2 Anemia due to scurvy.

Excludes: scurvy (E54)

D53.8 Other specified nutritional anaemias

Anemia associated with deficiency:

Excludes: malnutrition without mention of

anemia such as:

Copper deficiency (E61.0)

Molybdenum deficiency (E61.5)

Zinc deficiency (E60)

D53.9 Nutritional anemia, unspecified Simple chronic anemia.

Excludes: anemia NOS (D64.9)

HEMOLYTIC ANEMIA (D55-D59)

D55 Anemia due to enzyme disorders

Excludes: drug-induced enzyme deficiency anemia (D59.2)

D55.0 Anemia due to deficiency of glucose-6-phosphate dehydrogenase [G-6-PD]. Favism. G-6-PD-deficiency anemia

D55.1 Anemia due to other disorders of glutathione metabolism.

Anemia due to deficiency of enzymes (with the exception of G-6-PD) associated with hexose monophosphate [HMP]

metabolic pathway shunt. Hemolytic nonspherocytic anemia (hereditary) type 1

D55.2 Anemia due to disorders of glycolytic enzymes.

Hemolytic non-spherocytic (hereditary) type II

Due to hexokinase deficiency

Due to pyruvate kinase deficiency

Due to deficiency of triose phosphate isomerase

D55.3 Anemia due to disorders of nucleotide metabolism

D55.8 Other anemia due to enzyme disorders

D55.9 Anemia due to enzyme disorder, unspecified

D56 Thalassemia

Excludes: hydrops fetalis due to hemolytic disease (P56.-)

D56.1 Beta-thalassemia. Anemia Cooley. Severe beta thalassemia. Sickle cell beta thalassemia.

D56.3 Thalassemia trait

D56.4 Hereditary persistence of fetal hemoglobin [NPPH]

D56.9 Thalassemia, unspecified Mediterranean anemia (with other hemoglobinopathies)

Thalassemia (minor) (mixed) (with other hemoglobinopathies)

D57 Sickle cell disorders

Excludes: other hemoglobinopathies (D58.-)

sickle cell beta thalassemia (D56.1)

D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis

D57.1 Sickle cell anemia without crisis.

D57.2 Double heterozygous sickle cell disorders

D57.3 Sickle cell carrier. Carriage of hemoglobin S. Heterozygous hemoglobin S

D57.8 Other sickle cell disorders

D58 Other hereditary hemolytic anemias

D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.

Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome

D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)

D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.

Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.

Excludes: familial polycythemia (D75.0)

Hb-M disease (D74.0)

hereditary persistence of fetal hemoglobin (D56.4)

altitude-related polycythemia (D75.1)

D58.8 Other specified hereditary hemolytic anemias stomatocytosis

D58.9 Hereditary hemolytic anemia unspecified

D59 Acquired hemolytic anemia

D59.0 Drug-induced autoimmune hemolytic anemia.

If necessary, to identify the medicinal product, use an additional external cause code (class XX).

D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (heat type). Chronic disease caused by cold hemagglutinins.

Cold type (secondary) (symptomatic)

Thermal type (secondary) (symptomatic)

Excludes: Evans syndrome (D69.3)

hemolytic disease of fetus and newborn (P55.-)

paroxysmal cold hemoglobinuria (D59.6)

D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.

If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.

D59.3 Hemolytic uremic syndrome

D59.4 Other non-autoimmune hemolytic anemias.

If it is necessary to identify the cause, use an additional external cause code (class XX).

D59.5 Paroxysmal nocturnal hemoglobinuria[Marchiafava-Micheli].

D59.6 Hemoglobinuria due to hemolysis caused by other external causes.

Excludes: hemoglobinuria NOS (R82.3)

D59.8 Other acquired hemolytic anemias

D59.9 Acquired hemolytic anemia, unspecified Idiopathic hemolytic anemia, chronic

D60 Acquired pure red cell aplasia (erythroblastopenia)

Includes: red cell aplasia (acquired) (adults) (with thymoma)

D60.0 Chronic acquired pure red cell aplasia

D60.1 Transient acquired pure red cell aplasia

D60.8 Other acquired pure red cell aplasia

D60.9 Acquired pure red cell aplasia, unspecified

D61 Other aplastic anemias

Excludes: agranulocytosis (D70)

D61.0 Constitutional aplastic anemia.

Aplasia (pure) red cell:

Blackfan-Diamond Syndrome. Familial hypoplastic anemia. Anemia Fanconi. Pancytopenia with malformations

D61.1 Drug-induced aplastic anemia. If necessary, identify the drug

use an additional external cause code (class XX).

D61.2 Aplastic anemia due to other external agents.

If it is necessary to identify the cause, use an additional code of external causes (class XX).

D61.3 Idiopathic aplastic anemia

D61.8 Other specified aplastic anemias

D61.9 Aplastic anemia, unspecified Hypoplastic anemia NOS. hypoplasia bone marrow. Panmyeloftis

D62 Acute posthemorrhagic anemia

Excludes: congenital anemia due to fetal blood loss (P61.3)

D63 Anemia in chronic diseases classified elsewhere

D63.0 Anemia in neoplasms (C00-D48+)

D63.8 Anemia in other chronic diseases classified elsewhere

D64 Other anemias

With an excess of blasts (D46.2)

With transformation (D46.3)

With sideroblasts (D46.1)

Without sideroblasts (D46.0)

D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia

D64.1 Secondary sideroblastic anemia due to other diseases.

If necessary, to identify the disease, use an additional code.

D64.2 Secondary sideroblastic anemia due to medicines or toxins.

If it is necessary to identify the cause, use an additional code of external causes (class XX).

D64.3 Other sideroblastic anemias.

Pyridoxine-reactive, not elsewhere classified

D64.4 Congenital dyserythropoietic anemia. Dyshemopoietic anemia (congenital).

Excludes: Blackfan-Diamond syndrome (D61.0)

di Guglielmo's disease (C94.0)

D64.8 Other specified anemias. Pediatric pseudoleukemia. Leukoerythroblastic anemia

BLOOD COAGULATION DISORDERS, PURPLE AND OTHERS

HEMORRHAGIC CONDITIONS (D65-D69)

D65 Disseminated intravascular coagulation [defibrination syndrome]

Afibrinogenemia acquired. Consumption coagulopathy

Diffuse or disseminated intravascular coagulation

Fibrinolytic bleeding acquired

Excludes: defibrination syndrome (complicating):

Newborn (P60)

D66 Hereditary factor VIII deficiency

Factor VIII deficiency (with functional impairment)

Excludes: factor VIII deficiency with vascular disorder (D68.0)

D67 Hereditary factor IX deficiency

Factor IX (with functional impairment)

Thromboplastic component of plasma

D68 Other bleeding disorders

Abortion, ectopic or molar pregnancy (O00-O07, O08.1)

Pregnancy, childbirth and puerperium (O45.0, O46.0, O67.0, O72.3)

D68.0 Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular damage. Vascular hemophilia.

Excludes: fragility of capillaries hereditary (D69.8)

factor VIII deficiency:

With functional impairment (D66)

D68.1 Hereditary deficiency of factor XI. Hemophilia C. Plasma thromboplastin precursor deficiency

D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.

Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease

D68.3 Hemorrhagic disorders due to circulating anticoagulants in the blood. Hyperheparinemia.

If it is necessary to identify the anticoagulant used, use an additional external cause code.

D68.4 Acquired coagulation factor deficiency.

Coagulation factor deficiency due to:

Vitamin K deficiency

Excludes: vitamin K deficiency in newborn (P53)

D68.8 Other specified bleeding disorders Presence of an inhibitor of systemic lupus erythematosus

D68.9 Coagulation disorder, unspecified

D69 Purpura and other hemorrhagic conditions

Excludes: benign hypergammaglobulinemic purpura (D89.0)

cryoglobulinemic purpura (D89.1)

idiopathic (hemorrhagic) thrombocythemia (D47.3)

fulminant purpura (D65)

thrombotic thrombocytopenic purpura (M31.1)

D69.0 Allergic purpura.

D69.1 Qualitative defects in platelets. Bernard-Soulier [giant platelet] syndrome.

Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). thrombocytopathy.

Excludes: von Willebrand disease (D68.0)

D69.2 Other non-thrombocytopenic purpura.

D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome

D69.4 Other primary thrombocytopenias.

Excludes: thrombocytopenia with no radius(Q87.2)

transient neonatal thrombocytopenia (P61.0)

Wiskott-Aldrich syndrome (D82.0)

D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).

D69.6 Thrombocytopenia, unspecified

D69.8 Other specified haemorrhagic conditions Fragility of capillaries (hereditary). Vascular pseudohemophilia

D69.9 Hemorrhagic condition, unspecified

OTHER DISEASES OF THE BLOOD AND BLOOD-MAKE ORGANS (D70-D77)

D70 Agranulocytosis

Agranulocytic angina. Children's genetic agranulocytosis. Kostmann disease

If necessary, to identify the drug that caused neutropenia, use an additional external cause code (class XX).

Excludes: transient neonatal neutropenia (P61.5)

D71 Functional disorders of polymorphonuclear neutrophils

Defect of the receptor complex of the cell membrane. Chronic (children's) granulomatosis. Congenital dysphagocytosis

Progressive septic granulomatosis

D72 Other white blood cell disorders

Excludes: basophilia (D75.8)

immune disorders (D80-D89)

preleukemia (syndrome) (D46.9)

D72.0 Genetic abnormalities of leukocytes.

Anomaly (granulation) (granulocyte) or syndrome:

Excludes: Chediak-Higashi (-Steinbrink) syndrome (E70.3)

D72.8 Other specified disorders of white blood cells

Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). plasmacytosis

D72.9 White blood cell disorder, unspecified

D73 Diseases of the spleen

D73.0 Hyposplenism. Asplenia postoperative. Atrophy of the spleen.

Excludes: asplenia (congenital) (Q89.0)

D73.2 Chronic congestive splenomegaly

D73.5 Infarction of the spleen. Rupture of the spleen is non-traumatic. Torsion of the spleen.

Excludes: traumatic rupture of spleen (S36.0)

D73.8 Other diseases of the spleen. Fibrosis of the spleen NOS. Perisplenit. Spell NOS

D73.9 Disease of spleen, unspecified

D74 Methemoglobinemia

D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.

Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia

D74.8 Other methemoglobinemias Acquired methemoglobinemia (with sulfhemoglobinemia).

Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).

D74.9 Methemoglobinemia, unspecified

D75 Other diseases of the blood and blood-forming organs

Excluded: increase lymph nodes(R59.-)

hypergammaglobulinemia NOS (D89.2)

Mesenteric (acute) (chronic) (I88.0)

Excludes: hereditary ovalocytosis (D58.1)

D75.1 Secondary polycythemia.

Decreased plasma volume

D75.2 Essential thrombocytosis.

Excludes: essential (hemorrhagic) thrombocythemia (D47.3)

D75.8 Other specified diseases of the blood and blood-forming organs Basophilia

D75.9 Disorder of the blood and blood-forming organs, unspecified

D76 Certain diseases involving the lymphoreticular tissue and the reticulohistiocytic system

Excludes: Letterer-Siwe disease (C96.0)

malignant histiocytosis (C96.1)

reticuloendotheliosis or reticulosis:

Histiocytic medullary (C96.1)

D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.

Hand-Schuller-Chrisgen disease. Histiocytosis X (chronic)

D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.

Histiocytosis from mononuclear phagocytes other than Langerhans cells, NOS

D76.2 Hemophagocytic syndrome associated with infection.

If necessary, to identify an infectious agent or disease, use an additional code.

D76.3 Other histiocytic syndromes Reticulohistiocytoma (giant cell).

Sinus histiocytosis with massive lymphadenopathy. xanthogranuloma

D77 Other disorders of the blood and blood-forming organs in diseases classified elsewhere.

Fibrosis of the spleen in schistosomiasis [bilharzia] (B65.-)

SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)

Includes: defects in the complement system, immunodeficiency disorders excluding disease,

human immunodeficiency virus [HIV] sarcoidosis

Excl.: autoimmune diseases (systemic) NOS (M35.9)

functional disorders of polymorphonuclear neutrophils (D71)

human immunodeficiency virus [HIV] disease (B20-B24)

D80 Immunodeficiencies with predominant antibody deficiency

D80.0 Hereditary hypogammaglobulinemia.

Autosomal recessive agammaglobulinemia (Swiss type).

X-linked agammaglobulinemia [Bruton's] (with growth hormone deficiency)

D80.1 Non-familial hypogammaglobulinemia Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS

D80.2 Selective immunoglobulin A deficiency

D80.3 Selective immunoglobulin G subclass deficiency

D80.4 Selective immunoglobulin M deficiency

D80.5 Immunodeficiency with elevated immunoglobulin M

D80.6 Insufficiency of antibodies with close to normal levels of immunoglobulins or with hyperimmunoglobulinemia.

Antibody deficiency with hyperimmunoglobulinemia

D80.7 Transient hypogammaglobulinemia of children

D80.8 Other immunodeficiencies with a predominant defect in antibodies. Kappa light chain deficiency

D80.9 Immunodeficiency with predominant antibody defect, unspecified

D81 Combined immunodeficiencies

Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)

D81.0 Severe combined immunodeficiency with reticular dysgenesis

D81.1 Severe combined immunodeficiency with low T and B cell counts

D81.2 Severe combined immunodeficiency with low or normal B-cell count

D81.3 Adenosine deaminase deficiency

D81.5 Purine nucleoside phosphorylase deficiency

D81.6 Major histocompatibility complex class I deficiency. Naked lymphocyte syndrome

D81.7 Deficiency of class II molecules of major histocompatibility complex

D81.8 Other combined immunodeficiencies. Deficiency of biotin-dependent carboxylase

D81.9 Combined immunodeficiency, unspecified Severe combined immunodeficiency disorder NOS

D82 Immunodeficiencies associated with other significant defects

Excludes: atactic telangiectasia [Louis Bar] (G11.3)

D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema

D82.1 Di George's syndrome. Syndrome of the diverticulum of the pharynx.

Aplasia or hypoplasia with immune deficiency

D82.2 Immunodeficiency with dwarfism due to short limbs

D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.

X-linked lymphoproliferative disease

D82.4 Hyperimmunoglobulin E syndrome

D82.8 Immunodeficiency associated with other specified major defects

D82.9 Immunodeficiency associated with major defect, unspecified

D83 Common variable immunodeficiency

D83.0 Common variable immunodeficiency with predominant abnormalities in the number and functional activity of B cells

D83.1 Common variable immunodeficiency with predominance of disorders of immunoregulatory T cells

D83.2 Common variable immunodeficiency with autoantibodies to B or T cells

D83.8 Other common variable immunodeficiencies

D83.9 Common variable immunodeficiency, unspecified

D84 Other immunodeficiencies

D84.0 Lymphocyte functional antigen-1 defect

D84.1 Defect in the complement system. Deficiency of C1 esterase inhibitor

D84.8 Other specified immunodeficiency disorders

D84.9 Immunodeficiency, unspecified

D86 Sarcoidosis

D86.1 Sarcoidosis of lymph nodes

D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes

D86.8 Sarcoidosis of other specified and combined sites. Iridocyclitis in sarcoidosis (H22.1).

Multiple paralysis cranial nerves in sarcoidosis (G53.2)

Uveoparotitis fever [Herfordt's disease]

D86.9 Sarcoidosis, unspecified

D89 Other disorders involving the immune mechanism, not elsewhere classified

Excludes: hyperglobulinemia NOS (R77.1)

monoclonal gammopathy (D47.2)

graft failure and rejection (T86.-)

D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS

D89.2 Hypergammaglobulinemia, unspecified

D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified

D89.9 Disorder involving immune mechanism, unspecified Immune disease NOS

APLASTIC AND OTHER ANEMIA (D60-D64)

Excludes: refractory anemia:

• NOS (D46.4)
• with excess blasts (D46.2)
• with transformation (C92.0)
• with sideroblasts (D46.1)
• without sideroblasts (D46.0)

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is accepted as a unified normative document to account for morbidity, the reasons for the population's appeals to medical institutions of all departments, and the causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

Posthemorrhagic anemia

Posthemorrhagic anemia is a disease that is accompanied by a decrease in the number of red blood cells and hemoglobin concentration due to massive acute bleeding or as a result of even minor but chronic blood loss.

Hemoglobin is a protein complex of erythrocytes, which includes iron. Its main function is to carry oxygen with the blood flow to all organs and tissues without exception. If this process is disturbed, rather serious changes begin in the body, which are determined by the etiology and severity of anemia.

Depending on the underlying cause and course of posthemorrhagic anemia, acute and chronic forms are distinguished. In accordance with the international classification system, the disease is divided as follows:

• Secondary iron deficiency anemia after blood loss. ICD code 10 D.50
• Acute posthemorrhagic anemia. ICD code 10 D.62.
• Congenital anemia after hemorrhage in the fetus - P61.3.

AT clinical practice secondary iron deficiency anemia is also called posthemorrhagic chronic anemia.

Causes of the acute form of the disease

The main reason for the development of acute posthemorrhagic anemia is the loss of a large volume of blood over a short period of time, which occurred as a result of:

• Trauma that caused damage to the main arteries.
• Damage to large blood vessels during surgery.
• Rupture of the fallopian tube during the development of an ectopic pregnancy.
• diseases internal organs(most often the lungs, kidneys, heart, gastrointestinal tract), which can lead to acute massive internal bleeding.

In young children, the causes of acute posthemorrhagic anemia are most often injuries of the umbilical cord, congenital pathologies of the blood system, damage to the placenta during caesarean section, early detachment of the placenta, its presentation, birth trauma.

Causes of the chronic course of posthemorrhagic anemia

Chronic posthemorrhagic anemia develops as a result of small but regular bleeding. They may appear as a result of:

• Hemorrhoids, which is accompanied by fissures of the rectum, the appearance of blood impurities in the feces.
• Peptic ulcer of the stomach and duodenum.
• profuse menstruation, uterine bleeding while taking hormonal drugs.
• Vascular lesions by tumor cells.
• Chronic nosebleeds.
• Insignificant chronic blood loss in oncological diseases.
• Frequent blood sampling, catheter placement and other similar manipulations.
• Severe course of kidney disease with the release of blood in the urine.
• Helminth infestation.
• Cirrhosis of the liver, chronic liver failure.

The cause of chronic anemia of a similar etiology can also be hemorrhagic diathesis. This is a group of diseases in which a person has a tendency to bleed due to a violation of homeostasis.

Symptoms and picture of blood in anemia as a result of acute blood loss

The clinical picture of acute posthemorrhagic anemia develops very quickly. The main symptoms of this disease are accompanied by manifestations of general shock as a result of acute bleeding. In general, there are:

• Decreased blood pressure.
• Cloudiness or loss of consciousness.
• Strong pallor, bluish tint of the nasolabial fold.
• Thready pulse.
• Vomit.
• Excessive sweating, and there is a so-called cold sweat.
• Chills.
• Seizures.

If the bleeding has been successfully stopped, then such symptoms are replaced by dizziness, tinnitus, loss of orientation, blurred vision, shortness of breath, heart rhythm disturbances. Still pale skin and mucous membranes, low blood pressure.

Here you will find detailed information about the treatment methods.

Anemia-Symptoms and Treatment https://youtu.be/f5HXbNbBf5w

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Changes in the results of a blood test within a few days after stopping bleeding and the development of anemia are closely related to the compensation mechanisms that are "turned on" in the body in response to the loss of a large volume of blood. They can be divided into the following stages:

• The reflex phase, which develops on the first day after blood loss. Redistribution and centralization of blood circulation begins, peripheral vascular resistance increases. At the same time, a decrease in the number of erythrocytes is observed with normal values hemoglobin and hematocrit concentrations.
• The hydremic phase runs from the second to the fourth day. Extracellular fluid enters the vessels, glycogenolysis is activated in the liver, which leads to an increase in glucose content. Gradually, symptoms of anemia appear in the blood picture: the concentration of hemoglobin decreases, the hematocrit decreases. However, the value of the color index is still normal. Due to the activation of thrombus formation processes, the number of platelets decreases, and due to the loss of leukocytes during bleeding, leukopenia is observed.
• The bone marrow phase begins on the fifth day after bleeding. Insufficient supply of organs and tissues with oxygen activates the processes of hematopoiesis. In addition to low hemoglobin, hematocrit, tombocytopenia and leukopenia, a decrease in the total number of red blood cells is noted at this stage. When examining a blood smear, the presence of young forms of erythrocytes is noted: reticulocytes, sometimes erythroblasts.

Similar changes in the blood picture are described in many situational tasks for future doctors.

Symptoms and diagnosis of anemia in chronic bleeding

Chronic posthemorrhagic anemia in its symptoms is similar to iron deficiency, since regular light bleeding leads to a deficiency of this microelement. The course of this blood disease depends on its severity. It is determined depending on the concentration of hemoglobin. Normally, in men it is 135 - 160 g / l, and in women 120 - 140 g / l. In children, this value varies with age from 200 in infants to 150 in adolescents.

Degree of post-hemorrhagic chronic anemia Hemoglobin concentration

• 1 (light) degree 90 – 110 g/l
• 2 degree (moderate) 70 - 90 g/l
• Grade 3 (severe) below 70 g/l

At the initial stage of the development of the disease, patients complain of mild dizziness, flickering "flies" before the eyes, and increased fatigue. Externally noticeable pallor of the skin and mucous membranes.

At the second stage, a decrease in appetite, sometimes nausea, diarrhea, or, conversely, constipation, shortness of breath, is added to the listed symptoms. When listening to heart tones, doctors note heart murmurs characteristic of chronic posthemorrhagic anemia. The condition of the skin also changes: the skin becomes dry, flaky. Painful and inflamed cracks appear in the corners of the mouth. The condition of hair and nails worsens.

Severe anemia is manifested by numbness and tingling in the fingers and toes, specific taste preferences appear, for example, some patients begin to eat chalk, and the perception of smells changes. Very often this stage of chronic posthemorrhagic anemia is accompanied by rapidly progressive caries, stomatitis.

Diagnosis of posthemorrhagic anemia is based on the results clinical analysis blood. In addition to the decrease in the amount of hemoglobin and erythrocytes, characteristic of all types of anemia, a decrease in the color index is detected. Its value ranges from 0.5 - 0.6. In addition, in chronic posthemorrhagic anemia, mutated erythrocytes (microcytes and schizocytes) appear.

Treatment of anemia after massive blood loss

First of all, you need to stop the bleeding. If it is external, then it is necessary to apply a tourniquet, a pressure bandage and take the victim to the hospital. In addition to pallor, cyanosis and clouding of consciousness, severe dryness in the mouth testifies to internal bleeding. At home, it is impossible to help a person in this condition, so stopping internal bleeding is carried out only in a hospital.

After identifying the source and stopping the bleeding, it is urgent to restore the blood supply to the vessels. For this, reopoliglyukin, hemodez, polyglukin are prescribed. Acute blood loss also compensated by blood transfusion, taking into account the compatibility of the Rh factor and blood type. The volume of blood transfusion is usually 400 - 500 ml. These measures must be carried out very quickly, since a rapid loss of even ¼ of the total blood volume can be fatal.

After stopping the state of shock and carrying out all the necessary manipulations, they proceed to standard treatment, which consists in the introduction of iron preparations and enhanced nutrition to compensate for the deficiency of vitamins and microelements. Ferrum lek, ferlatum, maltofer are usually prescribed.

Usually, the restoration of a normal blood picture occurs after 6 to 8 weeks, but the use of drugs to normalize hematopoiesis continues for up to six months.

Treatment of chronic posthemorrhagic anemia

The first and most important step in the treatment of posthemorrhagic chronic anemia is to determine the source of bleeding and eliminate it. Even the loss of 10-15 ml of blood per day deprives the body of the entire amount of iron that was received with food that day.

A comprehensive examination of the patient is carried out, which necessarily includes consultations with a gastroenterologist, proctologist, hematologist, gynecologist for women, endocrinologist. After identifying the disease that caused the development of chronic posthemorrhagic anemia, its treatment immediately begins.

In parallel, drugs are prescribed that contain iron. For adults, its daily dose is about 100 - 150 mg. Complex agents are prescribed, which, in addition to iron, contain ascorbic acid and B vitamins, which contribute to its better absorption. These are sorbifer durules, ferroplex, fenyuls.

In severe post-hemorrhagic chronic anemia, to stimulate hematopoietic processes, transfusion of erythrocyte mass and injection of drugs with iron are indicated. Ferlatum, maltofer, likferr and similar medicines are prescribed.

Recovery after the main course of treatment

The duration of taking iron-containing drugs is determined by the doctor. In addition to the use of various drugs to restore the normal supply of oxygen to the organs and replenish iron stores in the body, good nutrition is very important.

In the diet of a person who has suffered posthemorrhagic anemia, proteins and iron must be present without fail. Preference should be given to meat, eggs, dairy products. The leaders in iron content are organ meats, especially beef liver, meat, fish, caviar, legumes, nuts, buckwheat and oatmeal.

When compiling a diet, attention should be paid not only to how much iron a particular product contains, but also to the degree of its absorption in the body. It increases with the use of vegetables and fruits that contain vitamins B and C. These are citrus fruits, black currants, raspberries, etc.

The course and therapy of posthemorrhagic anemia in children

Posthemorrhagic anemia in children is much more severe, especially its acute form. The clinical picture of this pathology practically does not differ from an adult, but develops faster. And if in an adult a certain amount of lost blood is compensated by the protective reactions of the body, then in a child this can be fatal.

Treatment of acute and chronic forms of posthemorrhagic anemia in children is the same. After identifying the cause and eliminating bleeding, a transfusion of erythrocyte mass is prescribed at the rate of 10-15 ml per kg of weight, iron preparations. Their dosage is calculated individually depending on the severity of anemia and the condition of the child.

For children around six months of age, early introduction of complementary foods is recommended, and should start with foods with a high iron content. Babies are shown the transition to special fortified mixtures. If the disease that led to the development of posthemorrhagic anemia is chronic and cannot be treated, then prophylactic courses of iron preparations must be repeated regularly.

With timely initiation of treatment and non-critical blood loss, the prognosis is generally favorable. After compensation for iron deficiency, the child quickly recovers.

At healthy person all basic blood values ​​should be normal, any deviation is a sign of the development of pathological processes. Anemia is characterized by a decrease in the number of red blood cells and low hemoglobin, the causes of the disease are congenital or acquired, often the disease occurs due to malnutrition.

Due to the reduction of red cells, anemia is called anemia.

Anemia - what is it?

- a disease that is manifested by a significant decrease in hemoglobin and the number of red blood cells. The ICD-10 disease code is D50–D89.

Anemia is not the main disease, pathology always develops against the background of malfunctions in the work of internal organs and systems.

Anemia classification

Since there are many reasons for the development of anemia, they appear different symptoms, each form requires a special drug therapy, the disease is classified according to certain indicators.

In any form of anemia, hemoglobin values ​​are always below acceptable limits, and the number of red blood cells may be normal or decrease.

By color index

color index- the level of saturation of red blood cells with hemoglobin. To calculate the erythrocyte index, hemoglobin is multiplied by 3, divided by the whole number of erythrocytes.

Classification:

With normochromic anemia, indicators only sometimes go beyond acceptable limits.

• hypochromic- color index up to 0.8 units;
• normochromic- color index 0.6–1.05 units;
• hyperchromic- the value of the color index exceeds 1.05 units.

The diameter of erythrocytes is 7.2–8 µm. An increase in size is a sign of vitamin B-9, B-12 deficiency, a decrease indicates a lack of iron.

According to the ability of the bone marrow to regenerate

The process of creating new cells occurs in the tissues of the main organ of the hematopoietic system, the main indicator of the normal functioning of the body is the presence in the blood of the required number of reticulocytes, primary red cells, the rate of their formation is called erythropoiesis.

Classification:

• regenerative - the number of reticulocytes is 0.5–2%, the regeneration rate is normal;
• hyporegenerative - there is a decrease in regenerative functions, the number of reticulocytes is 0.5%;
• hyperregenerative - an accelerated process of restoration of bone marrow tissues, reticulocytes in the blood more than 2%;
• aplastic - reticulocytes are absent, or their value does not exceed 0.2%.

It takes 2-3 hours to synthesize new red blood cells.

According to the mechanism of development of pathology

Anemia occurs as a result of severe blood loss, a violation of the formation of red blood cells or their rapid violation, according to the mechanism of development, the disease is divided into several categories.

Kinds:

• anemia due to severe blood loss, chronic bleeding;
• iron deficiency, renal, B12 and folic form, aplastic - these types of the disease arise due to problems in the process of hematopoiesis;
• with some autoimmune abnormalities, against the background of poor heredity, erythrocytes are intensively destroyed, anemia develops.

Short-term mild anemia occurs in women during menstruation, after childbirth. If there are no serious deviations in the body, to improve well-being, it is enough to adjust the diet, normalize the daily routine.

Severity of anemia

There are 3 levels of severity pathological condition, depending on how much the real values ​​of hemoglobin are below the permissible norm.

Hemoglobin norms

Before classifying anemia, test for hemoglobin levels

Degrees of severity:

• 1 degree - hemoglobin within 90 g / l;
• 2 degree - hemoglobin 70-90 g / l;
• Grade 3 - hemoglobin 70 g / l or less.

Mild forms of the disease are characterized by a slight deterioration in the condition, severe anemia poses a serious threat to the health of adults and children. pathological changes can be fatal.

Symptoms and clinical manifestations

With anemia, gas exchange is disturbed, against the background of a decrease in the number of red blood cells, they transport carbon dioxide and oxygen worse. One of the main signs of any type of disease is anemic syndrome - attacks of dizziness, drowsiness, fatigue, irritability, pale skin, headaches. A photo of sick people will allow you to determine the external signs of the disease.

Anemia due to erosive gastritis

Anemia causes pale skin

With a lack of iron, strange taste preferences appear - a person wants to eat lime, raw meat. Olfactory perversions are also observed - patients like the smell of dyes, gasoline.

Causes of anemia

Anemia is a consequence of massive or prolonged bleeding, a decrease in the rate of appearance of new red blood cells, and the rapid destruction of red blood cells. The disease often indicates a chronic or acute deficiency of iron, folic and ascorbic acid, vitamin B12, with excessive enthusiasm for strict diets, starvation.

Stomach ulcer can cause chronic blood loss

Pseudoanemia - a decrease in blood viscosity with the disappearance of edema, due to excessive fluid intake. Hidden anemia - thickening of the blood, occurs with profuse vomiting, diarrhea, excessive sweating, hemoglobin and red blood cells do not decrease.

Sometimes a person is diagnosed with mixed anemia, a decrease in hemoglobin of unknown origin, when it is not possible to identify the exact or only cause of the pathology even after a thorough examination.

A decrease in hemoglobin in children is often congenital, secondary anemia- a consequence of unbalanced nutrition, active growth in puberty.

Thalassemia - severe hereditary disease, occurs due to an increase in the rate of hemoglobin formation, erythrocytes have the shape of a target. Signs - yellowness, an earthy-green tint of the skin, an irregular shape of the skull and a violation of the structure of the bone tissue, deviations in mental and physical development, the eyes have a Mongoloid incision, the liver and spleen are enlarged.

The main signs of anemia are yellowness and whiteness.

Hemolytic anemia of newborns- occurs due to a Rh conflict, a child is diagnosed with severe edema, ascites at birth, there are a lot of immature erythrocytes in the blood. The degree of pathology is determined on the basis of hemoglobin and indirect bilirubin.

Spherocytic - a hereditary gene pathology in which erythrocytes are rounded, quickly destroyed in the spleen. The result is the formation of stones in gallbladder, jaundice, irritability, nervousness.

Which doctor should I contact?

With manifestations of anemia, it is necessary to start. After receiving the results of the initial diagnosis, further treatment will be dealt with,. If you suspect the presence of internal bleeding, tumors, urgent hospitalization is required.

Diagnostics

The main type of diagnostics- a detailed and complete blood test, using a hematological analyzer, determine the number of red blood cells, their structural features, the values ​​​​of the color index, hemoglobin, and recognize inflammatory processes.

To identify the pathology, take a full range of blood tests

Diagnostic methods:

• blood biochemistry;
• urine test to detect hemoglobin;
• examination of feces for the presence hidden blood, eggs of worms;
• fibrogastroduodenoscopy, colonoscopy - assessment of the state of the stomach and other organs of the gastrointestinal tract;
• myelogram;
• Ultrasound of the organs of the reproductive, digestive, respiratory systems;
• CT of the lungs, kidneys;
• fluorography;
• ECG, echocardiography;

Erythrocytes live on average 90-120 days, from decay (hemolysis) occurs inside the vessels, in the bone marrow, liver and spleen. Any failure in the work of these organs provokes the occurrence of anemia.

Anemia treatment

To raise hemoglobin, drugs are used in tablet form, in the form of injections, droppers, which eliminate the main cause of anemia, enhance the effect of drugs - folk methods.

When diagnosing internal bleeding, an operation is performed; in severe cases, transfusion or blood purification, bone marrow transplantation, and removal of the spleen are required.

Medications

Medications are selected based on the indicators of test results, the type and severity of anemia, the main diagnosis.

How to treat:

Aktiferrin - an iron-replenishing drug

• Aktiferrin, Ferlatum - iron preparations, prescribed in combination with vitamin C;
• intramuscular administration of vitamin B12;
• folic acid medicines;
• immunosuppressants, antimetabolites - Metoject, Ecoral;
• glucocorticosteroids - Prednisol, Medopred;
• various types of immunoglobulins;
• means for accelerating the process of formation of erythrocytes in stem cells - Epotal, Vepoks.

With severe blood loss, measures are taken to replenish the volume of circulating blood - with the help of droppers, an erythrocyte mass, a solution of Albumin, Polyglukin, Gelatinol, and glucose are injected.

Folk remedies

Alternative medicine methods normalize the values ​​of the main blood parameters in mild forms of anemia; in severe, chronic varieties of the disease, they are used only as an additional therapy after prior consultation with the attending physician.

Simple Recipes:

1. Mix in equal proportions the juice of black radish, carrots, beets, simmer the mixture in the oven at minimum heat for 3 hours. Dosage for adults - 15 ml, for children - 5 ml, take the medicine three times a day.
2. Grind 100 g of fresh wormwood, pour 1 liter of vodka, put in a dark place for 21 days. Take 5 drops before each meal.
3. To 200 ml of pomegranate juice add 100 ml of carrot, apple and lemon juice, 70 ml of liquid honey. Refrigerate the mixture for 48 hours. Drink 30 ml three times a day.
4. Grind 300 g of peeled garlic, pour 1 liter of vodka, put in a dark place for 3 weeks. Drink 5 ml before meals.
5. Mix 175 ml of aloe juice, 75 ml of honey and 450 ml of Cahors, shake, put in the refrigerator. Drink 30 ml three times a day before meals.

The easiest method for eliminating and preventing anemia is to regularly use an infusion of rose hips, 1 tbsp. l. crushed raw materials, brew 1 liter of boiling water, leave for 8 hours in a thermos, or a well-wrapped pan.

When not severe forms anemia in the season, use 2 kg of watermelon, if there are no contraindications.

Possible consequences and complications

Without proper and timely therapy against the background of anemia, it weakens significantly the immune system, the risk of developing severe viral and bacterial pathologies increases.

What is dangerous anemia:

• pulmonary, renal and heart failure;
• diseases of a neurological nature;
• deterioration of memory, concentration of attention;
• deformation of the skin, mucous membranes;
• deviations in mental and physical development in children;
• chronic diseases of the eyes, organs of the digestive and respiratory systems.

One of the consequences of anemia is memory impairment.

In severe forms of anemia, tissue hypoxia develops, which can cause hemorrhagic and cardiogenic shock, hypotension, coma, and death.

Features of anemia during pregnancy

All pregnant women are at risk, anemia is often diagnosed during this period, but hemoglobin and red blood cell count usually decrease slightly, general state normal. The reasons- an increase in the liquid component of the blood against the background of a decrease in the volume of blood cells.

Sometimes, against the background of frequent vomiting with toxicosis, with problems with iron absorption, true iron deficiency anemia occurs, pathology is observed when carrying two or more children, with frequent pregnancies.

Symptoms- fatigue, weakness, insomnia or drowsiness, severe shortness of breath, nausea, a tendency to faint. The skin becomes dry and pale, the nails break, the hair falls out badly. This condition can cause miscarriage, preeclampsia, premature delivery, childbirth is usually difficult. In pregnant women, the lower limit of hemoglobin level is 110 mg / l.

Basis of therapy- diet, the menu should have more offal, dietary meat, fish, 15-35 mg of iron should be consumed per day, depending on the duration of pregnancy. Additionally, preparations with ascorbic and folic acid, sulfate and iron hydroxide are prescribed.

If a woman was diagnosed with anemia during pregnancy, iron deficiency is often observed in a child in the first year of life.

Prevention

Proper, balanced nutrition will help reduce the likelihood of anemia - reduce the intake of animal fats, replace them with vegetable ones, avoid low-carbohydrate diets, eat more honey, buckwheat and oatmeal, vegetables, fruits, berries.

Regular sports will replenish your blood and prevent almost any disease.

All types of liver, beef tongue, beef and poultry, fish, peas, buckwheat porridge, beets, cherries and apples - all these foods are rich in iron, maintain hemoglobin levels at the proper level.

- a common disease, occurs in women 10 times more often than in men. Modern medicines, folk recipes effectively help to cope with the pathology, avoid complications, and the observance of simple preventive measures will reduce the risk of developing the disease.

Hypochromic anemia is a whole group of blood diseases that combines general symptom: Decreased color index value is less than 0.8. This indicates an insufficient concentration of hemoglobin in the erythrocyte. It plays a key role in the transport of oxygen to all cells, and its deficiency causes the development of hypoxia and its accompanying symptoms.

Classification

Depending on the reason for the decrease in the color index, several types of hypochromic anemia are distinguished, these are:

• Iron deficiency or hypochromic microcytic anemia is the most common cause of hemoglobin deficiency.
• Iron-rich anemia, it is also called sideroachrestic. With this type of disease, iron enters the body in sufficient quantities, but due to a violation of its absorption, the concentration of hemoglobin decreases.
• Iron-redistributive anemia occurs due to increased breakdown of red blood cells and the accumulation of iron in the form of ferrites. In this form, it is not included in the process of erythropoiesis.
• Anemia of mixed origin.

According to the generally accepted international classification, hypochromic anemia is classified as iron deficiency. They are assigned an ICD code 10 D.50

The reasons

The causes of hypochromic anemia vary depending on its type. So, the factors that contribute to the development of anemia with iron deficiency are:

• Chronic blood loss associated with menstrual bleeding in women, peptic ulcer of the stomach, damage to the rectum with hemorrhoids, etc.
• Increased iron intake, e.g. due to pregnancy, lactation, rapid growth during adolescence.
• Insufficient intake of iron from food.
• Violation of iron absorption in the gastrointestinal tract due to diseases of the digestive system, operations for resection of the stomach or intestines.

Iron-saturated anemia is rare. They can develop under the influence of hereditary congenital pathologies, such as porphyria, and also be acquired. The causes of hypochromic anemia of this type may be taking certain medications, poisoning with poisons, heavy metals, and alcohol. It should be noted that these diseases are often referred to as hemolytic diseases blood.

Iron-redistributive anemia is a companion of acute and chronic inflammatory processes, suppuration, abscesses, non-infectious diseases, for example, tumors.

Diagnosis and determination of the type of anemia

A blood test reveals signs that are characteristic of most of these diseases - this is a decrease in hemoglobin levels, the number of red blood cells. As mentioned above, a decrease in the value of the color index is characteristic of hypochromic anemia.

To determine the treatment regimen, it is necessary to diagnose the type of hypochromic anemia. Additional diagnostic criteria are the following parameters:

• Determination of the level of iron in the blood serum.
• Determination of the iron-binding capacity of serum.
• Measurement of the level of iron-containing protein ferritin.
• It is possible to determine the total level of iron in the body by counting sideroblasts and siderocytes. What it is? These are erythoid cells in the bone marrow that contain iron.

Summary table of these indicators for various types hypochromic anemia is presented below.

Symptoms

Doctors note that the clinical picture of the disease depends on the severity of its course. Depending on the concentration of hemoglobin, a mild degree is distinguished (Hb content is in the range of 90–110 g/l), moderate hypochromic anemia (hemoglobin concentration is 70–90 g/l) and a severe degree. As the amount of hemoglobin decreases, the severity of symptoms increases.

Hypochromic anemia is accompanied by:

• Dizziness, flashing "flies" before the eyes.
• Digestive disorders, which are manifested by constipation, diarrhea or nausea.
• Changes in taste and perception of smells, lack of appetite.
• Dryness and peeling of the skin, the appearance of painful cracks in the corners of the mouth, on the feet and between the fingers.
• Inflammation of the oral mucosa.
• Rapidly developing carious processes.
• Deterioration of the condition of hair and nails.
• The appearance of shortness of breath even with minimal physical activity.

Hypochromic anemia in children is manifested by tearfulness, fatigue, moodiness. Pediatricians say that a severe degree is characterized by a delay in psycho-emotional and physical development. Congenital forms of the disease are detected very quickly and require immediate treatment.

With a small but chronic iron loss, mild chronic hypochromic anemia develops, which is characterized by constant fatigue, lethargy, shortness of breath, decreased performance.

Treatment of iron deficiency anemia

Treatment of hypochromic anemia of any type begins with determining its type and etiology. Timely elimination of the cause of a decrease in hemoglobin concentration plays a key role in successful therapy. Then drugs are prescribed that promote recovery normal indicators blood and alleviate the condition of the patient.

For the treatment of iron deficiency anemia, iron preparations are used in the form of syrups, tablets or injections (in case of impaired absorption of iron in the digestive tract). These are ferrum lek, sorbifer durules, maltofer, sorbifer, etc. For adults, the dosage is 200 mg of iron per day, for children it is calculated depending on weight and is 1.5 - 2 mg / kg. To increase the absorption of iron, ascorbic acid is prescribed at a dose of 200 mg for every 30 mg of iron. In severe cases, red blood cell transfusion is indicated, taking into account the blood type and Rh factor. However, this is only used as a last resort.

So, with thalassemia, children from a very early age are given periodic blood transfusions, and in severe cases, bone marrow transplantation is done. Often, such forms of the disease are accompanied by an increase in the concentration of iron in the blood, so the appointment of drugs containing this trace element leads to a deterioration in the patient's condition.

Such patients are shown the use of the drug desferal, which helps to remove excess iron from the body. Dosage is calculated based on age and blood test results. Usually desferal is prescribed in parallel with ascorbic acid, which increases its effectiveness.

In general, with the development modern methods treatment and diagnosis therapy of any form of hypochromic anemia, even hereditary, is quite possible. A person can take maintenance courses of certain medications and lead a completely normal life.

Among various anemic conditions iron deficiency anemia are the most common and account for about 80% of all anemias.

Iron-deficiency anemia- hypochromic microcytic anemia, which develops as a result of an absolute decrease in iron stores in the body. Iron deficiency anemia occurs, as a rule, with chronic blood loss or insufficient intake of iron in the body.

According to the World Health Organization, every 3rd woman and every 6th man in the world (200 million people) suffer from iron deficiency anemia.

iron exchange
Iron is an essential biometal that plays an important role in the functioning of cells in many body systems. The biological significance of iron is determined by its ability to reversibly oxidize and reduce. This property ensures the participation of iron in the processes of tissue respiration. Iron makes up only 0.0065% of body weight. The body of a man weighing 70 kg contains approximately 3.5 g (50 mg/kg body weight) of iron. The iron content in the body of a woman weighing 60 kg is approximately 2.1 g (35 mg/kg of body weight). Iron compounds have a different structure, have a functional activity characteristic only for them, and play an important biological role. The most important iron-containing compounds include: hemoproteins, the structural component of which is heme (hemoglobin, myoglobin, cytochromes, catalase, peroxidase), non-heme group enzymes (succinate dehydrogenase, acetyl-CoA dehydrogenase, xanthine oxidase), ferritin, hemosiderin, transferrin. Iron is part of complex compounds and is distributed in the body as follows:
- heme iron - 70%;
- iron depot - 18% (intracellular accumulation in the form of ferritin and hemosiderin);
- functioning iron - 12% (myoglobin and iron-containing enzymes);
- transported iron - 0.1% (iron associated with transferrin).

There are two types of iron: heme and non-heme. Heme iron is part of hemoglobin. It is contained only in a small part of the diet (meat products), is well absorbed (by 20-30%), its absorption is practically not affected by other food components. Non-heme iron is in free ionic form - ferrous (Fe II) or ferric (Fe III). Most dietary iron is non-heme iron (found primarily in vegetables). The degree of its assimilation is lower than that of heme, and depends on a number of factors. From food, only divalent non-heme iron is absorbed. To “turn” ferric iron into ferrous, a reducing agent is needed, the role of which in most cases is played by ascorbic acid (vitamin C). In the process of absorption in the cells of the intestinal mucosa, ferrous iron Fe2 + turns into oxide Fe3 + and binds to a special carrier protein - transferrin, which transports iron to hematopoietic tissues and iron deposition sites.

The accumulation of iron is carried out by the proteins ferritin and hemosiderin. If necessary, iron can be actively released from ferritin and used for erythropoiesis. Hemosiderin is a ferritin derivative with a higher iron content. From hemosiderin, iron is released slowly. Beginning (prelatent) iron deficiency can be identified by a reduced concentration of ferritin even before the exhaustion of iron stores, while still maintaining normal concentrations of iron and transferrin in the blood serum.

What causes iron deficiency anemia:

The main etiopathogenetic factor in the development of iron deficiency anemia is iron deficiency. The most common causes of iron deficiency conditions are:
1. iron loss in chronic bleeding (most common cause reaching 80%):
- bleeding from the gastrointestinal tract: peptic ulcer, erosive gastritis, varicose veins esophageal veins, colonic diverticula, hookworm invasions, tumors, UC, hemorrhoids;
- long and heavy menstruation, endometriosis, fibromyoma;
- macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis disease, polycystic kidney disease, tumors of the kidneys and bladder;
- nasal, pulmonary bleeding;
- blood loss during hemodialysis;
- uncontrolled donation;
2. insufficient absorption of iron:
- resection of the small intestine;
- chronic enteritis;
- malabsorption syndrome;
- intestinal amyloidosis;
3. increased need for iron:
- intensive growth;
- pregnancy;
- the period of breastfeeding;
- sports activities;
4. insufficient intake of iron from food:
- newborns;
-- Small children;
- Vegetarianism.

Pathogenesis (what happens?) during iron deficiency anemia:

Pathogenetically, the development of an iron deficiency state can be divided into several stages:
1. prelatent iron deficiency (insufficiency of accumulation) - there is a decrease in the level of ferritin and a decrease in the iron content in the bone marrow, iron absorption is increased;
2. latent iron deficiency (iron-deficient erythropoiesis) - serum iron is additionally reduced, the concentration of transferrin is increased, the content of sideroblasts in the bone marrow is reduced;
3. severe iron deficiency = iron deficiency anemia - the concentration of hemoglobin, red blood cells and hematocrit is additionally reduced.

Symptoms of iron deficiency anemia:

During the period of latent iron deficiency, many subjective complaints and Clinical signs characteristic of iron deficiency anemia. Patients report general weakness, malaise, decreased performance. Already during this period, there may be a perversion of taste, dryness and tingling of the tongue, a violation of swallowing with a sensation foreign body in the throat, palpitations, shortness of breath.
An objective examination of patients reveals "small symptoms of iron deficiency": atrophy of the papillae of the tongue, cheilitis, dry skin and hair, brittle nails, burning and itching of the vulva. All these signs of violation of the trophism of epithelial tissues are associated with tissue sideropenia and hypoxia.

Patients with iron deficiency anemia note general weakness, fatigue, difficulty concentrating, and sometimes drowsiness. There is a headache, dizziness. With severe anemia, fainting is possible. These complaints, as a rule, do not depend on the degree of decrease in hemoglobin, but on the duration of the disease and the age of the patients.

Iron deficiency anemia is also characterized by changes in the skin, nails, and hair. The skin is usually pale, sometimes with a slight greenish tint (chlorosis) and with an easy blush of the cheeks, it becomes dry, flabby, flaky, cracks easily. Hair loses its luster, becomes gray, thinner, breaks easily, thins and turns gray early. Nail changes are specific: they become thin, dull, flatten, easily exfoliate and break, striation appears. With pronounced changes, the nails acquire a concave, spoon-shaped shape (koilonychia). In patients with iron deficiency anemia, muscle weakness occurs, which is not observed in other types of anemia. It is referred to as a manifestation of tissue sideropenia. Atrophic changes occur in the mucous membranes of the digestive canal, respiratory organs, and genital organs. Damage to the mucous membrane of the digestive canal is a typical sign of iron deficiency conditions.
There is a decrease in appetite. There is a need for sour, spicy, salty foods. In more severe cases, there are perversions of smell, taste (pica chlorotica): eating chalk, lime, raw cereals, pogophagy (an attraction to eating ice). Signs of tissue sideropenia quickly disappear after taking iron supplements.

Diagnosis of iron deficiency anemia:

Main landmarks in laboratory diagnostics iron deficiency anemia the following:
1. The average content of hemoglobin in an erythrocyte in picograms (norm 27-35 pg) is reduced. To calculate it, the color index is multiplied by 33.3. For example, with a color index of 0.7 x 33.3, the hemoglobin content is 23.3 pg.
2. The average concentration of hemoglobin in the erythrocyte is reduced; normally, it is 31-36 g / dl.
3. Hypochromia of erythrocytes is determined by microscopy of a smear of peripheral blood and is characterized by an increase in the zone of central enlightenment in the erythrocyte; Normally, the ratio of central enlightenment to peripheral darkening is 1:1; with iron deficiency anemia - 2 + 3: 1.
4. Microcytosis of erythrocytes - a decrease in their size.
5. Coloring of erythrocytes of different intensity - anisochromia; the presence of both hypo- and normochromic erythrocytes.
6. different shape erythrocytes - poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and the period of ferrotherapy) with iron deficiency anemia remains normal.
8. The content of leukocytes is also within the normal range (with the exception of cases of blood loss or oncopathology).
9. The content of platelets often remains within the normal range; moderate thrombocytosis is possible with blood loss at the time of the examination, and the platelet count decreases when blood loss due to thrombocytopenia is the basis of iron deficiency anemia (for example, with DIC, Werlhof's disease).
10. Reducing the number of siderocytes up to their disappearance (siderocyte is an erythrocyte containing iron granules). In order to standardize the production of peripheral blood smears, it is recommended to use special automatic devices; the resulting monolayer of cells improves the quality of their identification.

Blood chemistry:
1. Decreased iron content in the blood serum (normal in men 13-30 µmol/l, in women 12-25 µmol/l).
2. TIBC is increased (reflects the amount of iron that can be bound by free transferrin; TIBC is normal - 30-86 µmol / l).
3. Study of transferrin receptors by enzyme immunoassay; their level is increased in patients with iron deficiency anemia (in patients with anemia chronic diseases- normal or reduced, despite similar indicators of iron metabolism.
4. The latent iron-binding capacity of the blood serum is increased (determined by subtracting the content of serum iron).
5. The percentage of saturation of transferrin with iron (the ratio of the serum iron index to the total body fat; normally 16-50%) is reduced.
6. The level of serum ferritin is also reduced (normally 15-150 mcg/l).

At the same time, in patients with iron deficiency anemia, the number of transferrin receptors is increased and the level of erythropoietin in the blood serum is increased (compensatory reactions of hematopoiesis). The volume of erythropoietin secretion is inversely proportional to the oxygen transport capacity of the blood and is directly proportional to the oxygen demand of the blood. It should be borne in mind that the level of serum iron is higher in the morning; before and during menstruation, it is higher than after menstruation. The content of iron in the blood serum in the first weeks of pregnancy is higher than in its last trimester. The level of serum iron increases on the 2nd-4th day after treatment with iron-containing drugs, and then decreases. Significant consumption meat products on the eve of the study is accompanied by hypersideremia. These data must be taken into account when evaluating the results of a serum iron study. Equally important is the technique laboratory research rules for blood sampling. Thus, the test tubes in which blood is collected must first be washed with hydrochloric acid and bidistilled water.

Myelogram study reveals a moderate normoblastic reaction and a sharp decrease in the content of sideroblasts (erythrocaryocytes containing iron granules).

The iron stores in the body are judged by the results of the desferal test. In a healthy person after intravenous administration 500 mg of desferal is excreted in the urine from 0.8 to 1.2 mg of iron, while in a patient with iron deficiency anemia, iron excretion is reduced to 0.2 mg. The new domestic drug defericolixam is identical to desferal, but circulates in the blood longer and therefore more accurately reflects the level of iron stores in the body.

Based on the level of hemoglobin, iron deficiency anemia, like other forms of anemia, is divided into severe, moderate and mild anemia. With mild iron deficiency anemia, the hemoglobin concentration is below normal, but more than 90 g / l; with iron deficiency anemia medium degree hemoglobin content less than 90 g/l, but more than 70 g/l; with severe iron deficiency anemia, the hemoglobin concentration is less than 70 g / l. However, clinical signs of the severity of anemia (symptoms of a hypoxic nature) do not always correspond to the severity of anemia according to laboratory criteria. Therefore, a classification of anemia according to the severity of clinical symptoms has been proposed.

According to clinical manifestations, 5 degrees of severity of anemia are distinguished:
1. anemia without clinical manifestations;
2. anemic syndrome of moderate severity;
3. severe anemic syndrome;
4. anemic precoma;
5. anemic coma.

Moderate severity of anemia is characterized by general weakness, specific signs (for example, sideropenic or signs of vitamin B12 deficiency); with a pronounced degree of severity of anemia, palpitations, shortness of breath, dizziness, etc. appear. Precomatous and comatose states can develop in a matter of hours, which is especially characteristic of megaloblastic anemia.

Modern clinical researches show that among patients with iron deficiency anemia, laboratory and clinical heterogeneity is observed. So, in some patients with signs of iron deficiency anemia and concomitant inflammatory and infectious diseases the level of serum and erythrocyte ferritin does not decrease, however, after the elimination of the exacerbation of the underlying disease, their content decreases, which indicates the activation of macrophages in the processes of iron consumption. In some patients, the level of erythrocyte ferritin even increases, especially in patients with a long course of iron deficiency anemia, which leads to ineffective erythropoiesis. Sometimes there is an increase in the level of serum iron and erythrocyte ferritin, a decrease in serum transferrin. It is assumed that in these cases, the process of iron transfer to hemosynthetic cells is disrupted. In some cases, a deficiency of iron, vitamin B12 and folic acid is determined simultaneously.

Thus, even the level of serum iron does not always reflect the degree of iron deficiency in the body in the presence of other signs of iron deficiency anemia. Only the level of TIBC in iron deficiency anemia is always elevated. Therefore, none biochemical indicator, incl. OZHSS cannot be considered as an absolute diagnostic criterion with iron deficiency anemia. At the same time, the morphological characteristics of peripheral blood erythrocytes and computer analysis of the main parameters of erythrocytes are decisive in the screening diagnosis of iron deficiency anemia.

Diagnosis of iron deficiency conditions is difficult in cases where the hemoglobin content remains normal. Iron deficiency anemia develops in the presence of the same risk factors as in iron deficiency anemia, as well as in individuals with an increased physiological need for iron, primarily in premature infants in early age, in adolescents with a rapid increase in height and body weight, in blood donors, with alimentary dystrophy. In the first stage of iron deficiency clinical manifestations are absent, and iron deficiency is determined by the content of hemosiderin in bone marrow macrophages and by the absorption of radioactive iron in the gastrointestinal tract. At the second stage (latent iron deficiency), an increase in the concentration of protoporphyrin in erythrocytes is observed, the number of sideroblasts decreases, and morphological features(microcytosis, hypochromia of erythrocytes), the average content and concentration of hemoglobin in erythrocytes decreases, the level of serum and erythrocyte ferritin decreases, saturation of transferrin with iron. The level of hemoglobin in this stage remains quite high, and clinical signs are characterized by a decrease in exercise tolerance. The third stage is manifested by clear clinical and laboratory signs of anemia.

Examination of patients with iron deficiency anemia
To exclude anemia that has common features with iron deficiency anemia, and to identify the cause of iron deficiency, a complete clinical examination of the patient is necessary:

General blood analysis with the obligatory determination of the number of platelets, reticulocytes, the study of the morphology of erythrocytes.

Blood chemistry: determination of the level of iron, OZhSS, ferritin, bilirubin (bound and free), hemoglobin.

In all cases it is necessary examine bone marrow punctate before the appointment of vitamin B12 (primarily for differential diagnosis with megaloblastic anemia).

To identify the cause of iron deficiency anemia in women, a preliminary consultation with a gynecologist is required to exclude diseases of the uterus and its appendages, and in men, an examination by a proctologist to exclude bleeding hemorrhoids and a urologist to exclude prostate pathology.

Cases of extragenital endometriosis are known, for example in respiratory tract. In these cases, hemoptysis is observed; fibrobronchoscopy with histological examination of the biopsy of the bronchial mucosa allows you to establish a diagnosis.

The examination plan also includes X-ray and endoscopic examination of the stomach and intestines in order to exclude ulcers, tumors, incl. glomic, as well as polyps, diverticulum, Crohn's disease, ulcerative colitis etc. If pulmonary siderosis is suspected, radiography and tomography of the lungs are performed, sputum examination for alveolar macrophages containing hemosiderin; in rare cases it is necessary histological examination lung biopsy. If a kidney pathology is suspected, a general urinalysis, a blood serum test for urea and creatinine are necessary, and, if indicated, an ultrasound and X-ray examination of the kidneys. In some cases, it is necessary to exclude endocrine pathology: myxedema, in which iron deficiency can develop a second time due to damage small intestine; Polymyalgia rheumatica is a rare connective tissue disease in older women (less often in men), characterized by pain in the muscles of the shoulder or pelvic girdle without any objective changes in them, and in the blood test - anemia and an increase in ESR.

Differential diagnosis of iron deficiency anemia
When making a diagnosis of iron deficiency anemia, differential diagnosis with other hypochromic anemias.

Iron-redistributive anemia is a fairly common pathology and, in terms of frequency of development, ranks second among all anemias (after iron deficiency anemia). It develops in acute and chronic infectious and inflammatory diseases, sepsis, tuberculosis, rheumatoid arthritis, liver diseases, oncological diseases, ischemic heart disease, etc. The mechanism of development of hypochromic anemia in these conditions is associated with the redistribution of iron in the body (it is located mainly in the depot) and a violation of the mechanism of iron recycling from the depot. In the above diseases, the activation of the macrophage system occurs, when macrophages, under conditions of activation, firmly retain iron, thereby disrupting the process of its reutilization. AT general analysis blood, there is a moderate decrease in hemoglobin (<80 г/л).

The main differences from iron deficiency anemia are:
- elevated serum ferritin, indicating an increased iron content in the depot;
- the level of serum iron may remain within normal limits or be moderately reduced;
- TIBC remains within normal limits or decreases, which indicates the absence of serum Fe-starvation.

Iron-saturated anemia develops as a result of impaired heme synthesis, which is due to heredity or can be acquired. Heme is formed from protoporphyrin and iron in erythrokaryocytes. With iron-saturated anemia, there is a violation of the activity of enzymes involved in the synthesis of protoporphyrin. The consequence of this is a violation of heme synthesis. Iron that has not been used for heme synthesis is deposited in the form of ferritin in bone marrow macrophages, as well as in the form of hemosiderin in the skin, liver, pancreas, and myocardium, resulting in secondary hemosiderosis. Anemia, erythropenia, and a decrease in color index will be recorded in the general blood test.

Indicators of iron metabolism in the body are characterized by an increase in the concentration of ferritin and the level of serum iron, normal indicators of TIBC, and an increase in the saturation of transferrin with iron (in some cases it reaches 100%). Thus, the main biochemical indicators that allow assessing the state of iron metabolism in the body are ferritin, serum iron, TIBC, and % saturation of transferrin with iron.

The use of indicators of iron metabolism in the body allows the clinician to:
- to identify the presence and nature of violations of iron metabolism in the body;
- identify the presence of iron deficiency in the body at the preclinical stage;
- to carry out differential diagnostics of hypochromic anemias;
- evaluate the effectiveness of the therapy.

Treatment for iron deficiency anemia:

In all cases of iron deficiency anemia, it is necessary to establish the immediate cause of this condition and, if possible, eliminate it (most often, eliminate the source of blood loss or treat the underlying disease complicated by sideropenia).

Treatment of iron deficiency anemia should be pathogenetically substantiated, comprehensive and aimed not only at eliminating anemia as a symptom, but also at eliminating iron deficiency and replenishing its reserves in the body.

Treatment program for iron deficiency anemia:
- elimination of the cause of iron deficiency anemia;
- medical nutrition;
- ferrotherapy;
- prevention of relapses.

Patients with iron deficiency anemia are recommended a varied diet, including meat products (veal, liver) and vegetable products (beans, soybeans, parsley, peas, spinach, dried apricots, prunes, pomegranates, raisins, rice, buckwheat, bread). However, it is impossible to achieve an antianemic effect with diet alone. Even if the patient eats high-calorie foods containing animal protein, iron salts, vitamins, microelements, iron absorption can be achieved no more than 3-5 mg per day. It is necessary to use iron preparations. Currently, the doctor has a large arsenal of iron preparations, characterized by different composition and properties, the amount of iron they contain, the presence of additional components that affect the pharmacokinetics of the drug, and various dosage forms.

According to the recommendations developed by WHO, when prescribing iron preparations, preference is given to preparations containing ferrous iron. The daily dose should reach 2 mg/kg of elemental iron in adults. The total duration of treatment is at least three months (sometimes up to 4-6 months). An ideal iron-containing preparation should have a minimum number of side effects, have a simple regimen of administration, the best ratio of effectiveness / price, optimal iron content, preferably the presence of factors that enhance absorption and stimulate hematopoiesis.

Indications for parenteral administration of iron preparations occur with intolerance to all oral preparations, malabsorption (ulcerative colitis, enteritis), peptic ulcer of the stomach and duodenum during an exacerbation, with severe anemia and the vital need for rapid replenishment of iron deficiency. The effectiveness of iron preparations is judged by changes in laboratory parameters over time. By the 5th-7th day of treatment, the number of reticulocytes increases by 1.5-2 times compared with the initial data. Starting from the 10th day of therapy, the hemoglobin content increases.

Given the prooxidant and lysosomotropic effect of iron preparations, their parenteral administration can be combined with intravenous drip administration of rheopolyglucin (400 ml once a week), which helps protect the cell and avoid macrophage overload with iron. Taking into account significant changes in the functional state of the erythrocyte membrane, activation of lipid peroxidation and a decrease in the antioxidant protection of erythrocytes in iron deficiency anemia, it is necessary to introduce antioxidants, membrane stabilizers, cytoprotectors, antihypoxants, such as a-tocopherol up to 100-150 mg per day (or ascorutin, vitamin A, vitamin C, lipostabil, methionine, mildronate, etc.), and also combined with vitamins B1, B2, B6, B15, lipoic acid. In some cases, it is advisable to use ceruloplasmin.

List of drugs that are used in the treatment of iron deficiency anemia: