Chronic iron deficiency anemia ICD 10. D50 Iron deficiency anemia. D62 Acute posthemorrhagic anemia

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

Excluded: 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 diseases, nutritional and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), trauma, poisoning and certain other consequences of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)

This class contains the following blocks:

D50-D53 Anemia associated with nutrition

D55-D59 Hemolytic anemias

D60-D64 Aplastic and other anemias

D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions

D70-D77 Other diseases of the blood and hematopoietic organs

D80-D89 Selected disorders involving the immune mechanism

The following categories are marked with an asterisk:

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

NUTRITION-RELATED 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. Anemia of vegetarians

D51.8 Other vitamin B12 deficiency anemias

D51.9 Vitamin B12 deficiency anemia, unspecified

D52 Folate deficiency anemia

D52.0 Folate deficiency anemia associated with nutrition. Megaloblastic nutritional anemia

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

use an additional external cause code (class XX)

D52.8 Other folate deficiency anemias

D52.9 Folate deficiency anemia, unspecified. Anemia due to insufficient intake of folic acid, NOS

D53 Other diet-related anemias

Includes: megaloblastic anemia not responding to vitamin therapy

nom B12 or folate

D53.0 Anemia due to protein deficiency. Anemia due to amino acid deficiency.

Excludes: Lesch-Nychen syndrome (E79.1)

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

Excludes: DiGuglielmo disease (C94.0)

D53.2 Anemia due to scurvy.

Excludes: scurvy (E54)

D53.8 Other specified anemias associated with nutrition.

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 Diet-related 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 glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6-PD deficiency anemia

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

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

bypass of the metabolic pathway. 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 triosephosphate isomerase deficiency

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. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.

D56.3 Carriage of thalassemia trait

D56.4 Hereditary persistence of fetal hemoglobin [HFH]

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

Thalassemia minor (mixed) (with other hemoglobinopathy)

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 Carriage of the sickle cell trait. 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 it is necessary to identify the drug, use an additional code for external causes (class XX).

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

Cold type (secondary) (symptomatic)

Thermal type (secondary) (symptomatic)

Excludes: Evans syndrome (D69.3)

hemolytic disease of the 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 drug, use an additional code for external causes (class XX).

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. Chronic idiopathic hemolytic anemia

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 aplasias

D60.9 Acquired pure red cell aplasia, unspecified

D61 Other aplastic anemias

Excluded: agranulocytosis (D70)

D61.0 Constitutional aplastic anemia.

Aplasia (pure) red cell:

Blackfan-Diamond syndrome. Familial hypoplastic anemia. Fanconi anemia. Pancytopenia with developmental defects

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

use an additional code for external causes (class XX).

D61.2 Aplastic anemia caused by 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. Bone marrow hypoplasia. Panmyelophthisis

D62 Acute posthemorrhagic anemia

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

D63 Anemia in chronic diseases classified elsewhere

D63.0 Anemia due to neoplasms (C00-D48+)

D63.8 Anemia in other chronic diseases classified elsewhere

D64 Other anemias

With excess blasts (D46.2)

With transformation (D46.3)

With sideroblasts (D46.1)

No sideroblasts (D46.0)

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

D64.1 Secondary sideroblastic anemia due to other diseases.

If necessary, an additional code is used to identify the disease.

D64.2 Secondary sideroblastic anemia caused by drugs 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. Dyshematopoietic anemia (congenital).

Excludes: Blackfan-Diamond syndrome (D61.0)

DiGuglielmo disease (C94.0)

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

BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS

HEMORRHAGIC CONDITIONS (D65-D69)

D65 Disseminated intravascular coagulation [defibration syndrome]

Afibrinogenemia acquired. Consumptive coagulopathy

Diffuse or disseminated intravascular coagulation

Acquired fibrinolytic bleeding

Excluded: defibration syndrome (complicating):

In a 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 plasma component

D68 Other bleeding disorders

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

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

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

Excludes: hereditary capillary fragility (D69.8)

factor VIII deficiency:

With functional impairment (D66)

D68.1 Hereditary factor XI deficiency. 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 caused by anticoagulants circulating in the blood. Hyperheparinemia.

If necessary, 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 the newborn (P53)

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

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)

lightning purple (D65)

thrombotic thrombocytopenic purpura (M31.1)

D69.0 Allergic purpura.

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

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 absent 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 hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia

D69.9 Hemorrhagic condition, unspecified

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

D70 Agranulocytosis

Agranulocytic tonsillitis. Children's genetic agranulocytosis. Kostmann's disease

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

Excludes: transient neonatal neutropenia (P61.5)

D71 Functional disorders of polymorphonuclear neutrophils

Defect of the cell membrane receptor complex. 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:

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

D72.8 Other specified white blood cell disorders.

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

D72.9 White blood cell disorder, unspecified

D73 Diseases of the spleen

D73.0 Hyposplenism. Postoperative asplenia. Atrophy of the spleen.

Excludes: asplenia (congenital) (Q89.0)

D73.2 Chronic congestive splenomegaly

D73.5 Splenic infarction. Splenic rupture is non-traumatic. Torsion of the spleen.

Excludes: traumatic splenic rupture (S36.0)

D73.8 Other diseases of the spleen. Splenic fibrosis NOS. Perisplenitis. Splenitis NOS

D73.9 Disease of the spleen, unspecified

D74 Methemoglobinemia

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

Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia

D74.8 Other methemoglobinemia. 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 hematopoietic organs

Excludes: swollen 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 hematopoietic organs. Basophilia

D75.9 Disease of the blood and hematopoietic organs, unspecified

D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system

Excludes: Letterer-Sieve 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-Schueller-Crisgen disease. Histiocytosis X (chronic)

D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.

Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS

D76.2 Hemophagocytic syndrome associated with infection.

If it is necessary to identify an infectious pathogen or disease, an additional code is used.

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

Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma

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

Splenic fibrosis in schistosomiasis [bilharzia] (B65. -)

SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)

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

caused by human immunodeficiency virus [HIV] sarcoidosis

Excludes: 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] (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 deficiency of immunoglobulin G subclasses

D80.4 Selective immunoglobulin M deficiency

D80.5 Immunodeficiency with increased levels of immunoglobulin M

D80.6 Antibody deficiency with immunoglobulin levels close to normal or with hyperimmunoglobulinemia.

Antibody deficiency with hyperimmunoglobulinemia

D80.7 Transient hypogammaglobulinemia of children

D80.8 Other immunodeficiencies with a predominant antibody defect. 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 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome

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

D81.8 Other combined immunodeficiencies. Biotin-dependent carboxylase deficiency

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

D82 Immunodeficiencies associated with other significant defects

Excludes: ataxic telangiectasia [Louis-Bart] (G11.3)

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

D82.1 Di Georg syndrome. Pharyngeal diverticulum syndrome.

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 significant defects

D82.9 Immunodeficiency associated with significant defect, unspecified

D83 Common variable immunodeficiency

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

D83.1 General variable immunodeficiency with a 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. C1 esterase inhibitor deficiency

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 localizations. Iridocyclitis in sarcoidosis (H22.1).

Multiple cranial nerve palsies in sarcoidosis (G53.2)

Uveoparotitic 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)

non-engraftment and graft 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 the immune mechanism, unspecified. Immune disease NOS

APLASTIC AND OTHER ANEMIA (D60-D64)

Excluded: 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, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and 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. No. 170

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

With changes and additions from 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 an erythrocyte that contains iron. Its main function is to transport oxygen through the bloodstream to all organs and tissues without exception. When this process is disrupted, quite serious changes begin in the body, which are determined by the etiology and severity of anemia.

Depending on the root 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 10 code D.50
• Acute posthemorrhagic anemia. ICD 10 code D.62.
• Congenital anemia after fetal bleeding – P61.3.

In 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 of the 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 umbilical cord injuries, congenital pathologies of the blood system, damage to the placenta during cesarean section, early placental abruption, placental previa, and birth trauma.

Causes of chronic posthemorrhagic anemia

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

• Hemorrhoids, which are accompanied by cracks in the rectum and the appearance of blood in the stool.
• Peptic ulcer of the stomach and duodenum.
• Heavy menstruation, uterine bleeding while taking hormonal medications.
• Damage to blood vessels by tumor cells.
• Chronic nosebleeds.
• Minor chronic blood loss in cancer.
• Frequent blood draws, catheter installations and other similar manipulations.
• Severe kidney disease with bleeding in the urine.
• Helminth infestation.
• Liver cirrhosis, chronic liver failure.

Chronic anemia of this etiology can also be caused by hemorrhagic diathesis. This is a group of diseases in which a person has a tendency to bleed due to disruption of homeostasis.

Symptoms and blood picture of anemia due to acute blood loss

The clinical picture of acute posthemorrhagic anemia develops very quickly. The main symptoms of this disease include manifestations of general shock as a result of acute bleeding. In general, the following are observed:

• Reduced blood pressure.
• Cloudiness or loss of consciousness.
• Severe pallor, bluish tint of the nasolabial fold.
• Thready pulse.
• Vomit.
• Increased sweating, and so-called cold sweat is observed.
• Chills.
• Cramps.

If the bleeding was successfully stopped, then such symptoms are replaced by dizziness, tinnitus, loss of orientation, blurred vision, shortness of breath, and irregular heartbeat. Pallor of the skin and mucous membranes and low blood pressure still persist.

Here you will find detailed information about treatment methods

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Changes in blood test results within a few days after bleeding has stopped and the development of anemia are closely related to compensation mechanisms that “turn 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. In this case, a decrease in the number of red blood cells is observed at normal values ​​​​of hemoglobin concentration and hematocrit.
• The hydremic phase occurs 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 color index value 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 oxygen supply to organs and tissues activates hematopoietic processes. In addition to decreased hemoglobin, hematocrit, thrombocytopenia and leukopenia, at this stage there is a decrease in the total number of red blood cells. When examining a blood smear, the presence of young forms of red blood cells 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 is similar in its symptoms to iron deficiency, since regular, mild 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 depending on age from 200 in infants to 150 in adolescents.

Degree of posthemorrhagic chronic anemia Hemoglobin concentration

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

At the initial stage of development of the disease, patients complain of slight dizziness, flashing “spots” before the eyes, and increased fatigue. Externally, pallor of the skin and mucous membranes is noticeable.

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

A severe degree of anemia is manifested by numbness and a tingling feeling 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 progressing caries and stomatitis.

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

Treatment of anemia after massive blood loss

First of all, it is necessary to stop the bleeding. If it is external, then it is necessary to apply a tourniquet and a pressure bandage and take the victim to the hospital. In addition to pallor, cyanosis and confusion, internal bleeding is indicated by severe dry mouth. It is impossible to help a person in this condition at home, so stopping internal bleeding is carried out only in a hospital setting.

After identifying the source and stopping the bleeding, it is urgently necessary to restore the blood supply to the vessels. For this purpose, rheopolyglucin, hemodez, polyglucin are prescribed. Acute blood loss is also compensated by blood transfusion, taking into account the compatibility of the Rh factor and blood group. 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 of the administration of iron supplements and enhanced nutrition to compensate for the deficiency of vitamins and microelements. Ferrum lek, ferlatum, maltofer are usually prescribed.

Typically, restoration of a normal blood picture occurs after 6–8 weeks, but the use of medications 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 its elimination. Even the loss of 10 - 15 ml of blood per day deprives the body of the entire amount of iron that was received during that day with food.

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

At the same time, medications that contain iron are prescribed. For adults, its daily dose is about 100 – 150 mg. Complex products are prescribed that, in addition to iron, contain ascorbic acid and B vitamins, which promote its better absorption. These are sorbifer durules, ferroplex, fenyuls.

In severe cases of posthemorrhagic chronic anemia, red blood cell transfusion and injection of drugs with iron are indicated to stimulate hematopoietic processes. Ferlatum, maltofer, likferr and similar medications 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 medications to restore normal oxygen supply to organs and replenish iron reserves in the body, proper nutrition is very important.

The diet of a person who has suffered posthemorrhagic anemia must contain proteins and iron. Preference should be given to meat, eggs, and dairy products. The leaders in iron content are meat by-products, especially beef liver, meat, fish, caviar, legumes, nuts, buckwheat and oatmeal.

When creating 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 consumption of vegetables and fruits that contain vitamins B and C. These are citrus fruits, black currants, raspberries, etc.

Course and treatment of posthemorrhagic anemia in children

Posthemorrhagic anemia in children is much more severe, especially its acute form. The clinical picture of this pathology is practically no different from that of an adult, but develops faster. And if in an adult a certain volume of lost blood is compensated by the body’s protective reactions, then in a child this can lead to death.

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

For children aged about six months, early introduction of complementary foods is recommended, and you should start with foods with a high iron content. Infants are advised to switch to special fortified formulas. If the disease that led to the development of posthemorrhagic anemia is chronic and cannot be treated, then preventive courses of iron supplements 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.

Anemia is one of the most common blood diseases among both adults and children.

To complete the medical documentation of a patient with anemia of any etiology, the doctor uses the anemia code according to ICD 10. There are different forms of the disease depending on the cause that led to a decrease in hemoglobin and red blood cells in the blood. Anemia can be iron deficiency, folate deficiency, B-12 deficiency, hemolytic, aplastic and unspecified.

Causes, clinical picture and treatment of the pathological condition

The general mechanism of development for any type of disease is a disruption in the functioning of the hematopoietic organs due to a chronic lack of certain nutrients or, in some cases, due to the rapid destruction of blood cells in the bloodstream. Immune disorders and exposure to toxic substances also play an important role.

In ICD 10, anemia is classified as a blood disease and has code D50-D64.

The main clinical symptoms are:

• weakness;
• pallor;
• dizziness;
• pathological changes in taste;
• pathological changes in the skin;
• headache;
• digestive problems;
• intoxication (with hemolytic forms).

Treatment is carried out depending on the cause of the pathological decrease in hemoglobin and red blood cells. It is imperative to choose the right diet and regimen for the patient. Unspecified anemia requires an extended comprehensive examination of the patient’s body and symptomatic treatment in the initial stages.

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 reserves in the body. Iron deficiency anemia occurs, as a rule, with chronic blood loss or insufficient intake of iron into 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 metabolism
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 body weight). Iron compounds have different structures, have unique functional activity 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), enzymes of the non-heme group (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 bound to 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 (20-30%), its absorption is practically not affected by other food components. Non-heme iron is found in free ionic form - ferrous (Fe II) or ferric iron (Fe III). Most dietary iron is non-heme (found primarily in vegetables). The degree of its absorption is lower than that of heme and depends on a number of factors. Only divalent non-heme iron is absorbed from food. To “convert” ferric iron into divalent iron, a reducing agent is needed, the role of which in most cases is played by ascorbic acid (vitamin C). During absorption in the cells of the intestinal mucosa, ferrous iron Fe2+ is converted into oxide Fe3+ and binds to a special carrier protein - transferrin, which transports iron to hematopoietic tissues and sites of iron deposition.

Iron accumulation 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 derivative of ferritin with a higher iron content. Iron is released slowly from hemosiderin. Incipient (prelatent) iron deficiency can be determined by a reduced concentration of ferritin even before the depletion 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 due to chronic bleeding (the most common cause, reaching 80%):
- bleeding from the gastrointestinal tract: peptic ulcer, erosive gastritis, esophageal varicose veins, colon diverticula, hookworm infestations, tumors, ulcerative colitis, hemorrhoids;
- long and heavy menstruation, endometriosis, fibroids;
-- macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis, polycystic kidney disease, kidney and bladder tumors;
- nosebleeds, 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;
- period of breastfeeding;
- playing sports;
4. insufficient intake of iron from food:
-- newborns;
-- Small children;
-- vegetarianism.

Pathogenesis (what happens?) during Iron deficiency anemia:

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

Symptoms of Iron Deficiency Anemia:

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

Patients with iron deficiency anemia report general weakness, fatigue, difficulty concentrating, and sometimes drowsiness. Headache and dizziness appear. Severe anemia may cause fainting. 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 on the cheeks, it becomes dry, flabby, peels, and cracks easily form. Hair loses its shine, turns grey, thins, breaks easily, thins and turns gray early. Changes in nails are specific: they become thin, matte, flattened, easily peel and break, and striations appear. With pronounced changes, the nails acquire a concave, spoon-shaped shape (koilonychia). Patients with iron deficiency anemia experience muscle weakness, which is not observed in other types of anemia. It is classified 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, distortions of smell and taste (pica chlorotica) are observed: eating chalk, lime, raw cereals, pogophagia (craving for eating ice). Signs of tissue sideropenia quickly disappear after taking iron supplements.

Diagnosis of Iron Deficiency Anemia:

Basic guidelines in laboratory diagnosis of iron deficiency anemia the following:
1. The average hemoglobin content in an erythrocyte in picograms (normal 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 peripheral blood smear and is characterized by an increase in the zone of central clearing in the erythrocyte; Normally, the ratio of central clearing to peripheral darkening is 1:1; for iron deficiency anemia - 2+3:1.
4. Microcytosis of erythrocytes - reduction in their size.
5. Coloring of erythrocytes of different intensity - anisochromia; the presence of both hypo- and normochromic red blood cells.
6. Different shapes of red blood cells - poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and a period of ferrotherapy) in iron deficiency anemia remains normal.
8. The leukocyte count is also within normal limits (except in cases of blood loss or cancer pathology).
9. The platelet count often remains within normal limits; moderate thrombocytosis is possible with blood loss at the time of examination, and the platelet count decreases when the basis of iron deficiency anemia is blood loss due to thrombocytopenia (for example, with DIC syndrome, Werlhof's disease).
10. Reducing the number of siderocytes until they disappear (a 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 increases the quality of their identification.

Blood chemistry:
1. Decrease in iron content in blood serum (normally in men 13-30 µmol/l, in women 12-25 µmol/l).
2. The total life-value percentage is increased (reflects the amount of iron that can be bound due to free transferrin; the normal level of total life-value percentage is 30-86 µmol/l).
3. Study of transferrin receptors using the enzyme immunoassay method; their level is increased in patients with iron deficiency anemia (in patients with anemia of chronic diseases - normal or reduced, despite similar indicators of iron metabolism.
4. The latent iron-binding capacity of blood serum is increased (determined by subtracting the serum iron content from the TLC indicators).
5. The percentage of transferrin saturation with iron (the ratio of the serum iron index to the total life-saving value; 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 directly proportional to the oxygen demand of the blood. It should be taken into account that serum iron levels are higher in the morning; before and during menstruation it is higher than after menstruation. The iron content in blood serum in the first weeks of pregnancy is higher than in its last trimester. Serum iron levels increase on days 2-4 after treatment with iron-containing drugs and then decrease. Significant consumption of meat products on the eve of the study is accompanied by hypersideremia. These data must be taken into account when assessing the results of serum iron studies. It is equally important to follow laboratory testing techniques and blood sampling rules. Thus, the tubes in which blood is collected must first be washed with hydrochloric acid and double-distilled water.

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

Iron reserves in the body are judged by the results of the desferal test. In a healthy person, after intravenous administration of 500 mg of desferal, 0.8 to 1.2 mg of iron is excreted in the urine, while in a patient with iron deficiency anemia, iron excretion decreases 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 reserves in the body.

Taking into account 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 moderate iron deficiency anemia, the hemoglobin content is 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.

Based on clinical manifestations, there are 5 degrees of severity of anemia:
1. anemia without clinical manifestations;
2. moderate anemic syndrome;
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. Precomatose and comatose states can develop in a matter of hours, which is especially typical for megaloblastic anemia.

Modern clinical studies show that laboratory and clinical heterogeneity is observed among patients with iron deficiency anemia. Thus, 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, but after the exacerbation of the underlying disease is eliminated, their content drops, 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 long-term 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 heme-synthesizing cells is disrupted. In some cases, a deficiency of iron, vitamin B12 and folic acid is simultaneously determined.

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 THC in iron deficiency anemia is always elevated. Therefore, not a single biochemical indicator, incl. OZHSS cannot be considered as an absolute diagnostic criterion for 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 level remains normal. Iron deficiency anemia develops in the presence of the same risk factors as for iron deficiency anemia, as well as in individuals with an increased physiological need for iron, especially in premature infants at an early age, in adolescents with a rapid increase in height and body weight, in blood donors, with nutritional dystrophy. At the first stage of iron deficiency, there are no clinical manifestations, 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, morphological signs appear (microcytosis, hypochromia of erythrocytes), the average content and concentration of hemoglobin in erythrocytes decreases, the level of serum and erythrocyte ferritin, and transferrin saturation with iron decrease. The hemoglobin level at this stage remains quite high, and clinical signs are characterized by a decrease in exercise tolerance. The third stage is manifested by obvious 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, and the study of erythrocyte morphology.

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

In all cases it is necessary examine bone marrow aspirate before prescribing 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 pathology of the prostate gland.

There are known cases of extragenital endometriosis, for example in the respiratory tract. In these cases, hemoptysis is observed; fiberoptic bronchoscopy with histological examination of a biopsy of the bronchial mucosa makes it possible to establish a diagnosis.

The examination plan also includes x-ray and endoscopic examination of the stomach and intestines to exclude ulcers, tumors, incl. glomic, as well as polyps, diverticulum, Crohn's disease, ulcerative colitis, etc. If pulmonary siderosis is suspected, X-ray and tomography of the lungs and sputum examination for alveolar macrophages containing hemosiderin are performed; in rare cases, histological examination of a lung biopsy is necessary. If kidney pathology is suspected, a general urine test, blood serum testing for urea and creatinine are required, 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 secondary to damage to the 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 a blood test - anemia and an increase in ESR.

Differential diagnosis of iron deficiency anemia
When diagnosing iron deficiency anemia, it is necessary to carry out a differential diagnosis with other hypochromic anemias.

Iron redistribution anemia is a fairly common pathology and in terms of frequency of development it 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, cancer, 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 mechanism for recycling iron from the depot. In the above diseases, activation of the macrophage system occurs, when macrophages, under activation conditions, firmly retain iron, thereby disrupting the process of its reutilization. A general blood test shows a moderate decrease in hemoglobin (<80 г/л).

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

Iron-saturated anemia develops as a result of a violation of heme synthesis, which is caused by heredity or can be acquired. Heme is formed from protoporphyrin and iron in erythrokaryocytes. In iron-saturated anemia, the activity of enzymes involved in the synthesis of protoporphyrin occurs. The consequence of this is a violation of heme synthesis. Iron, which was not used for heme synthesis, is deposited in the form of ferritin in macrophages of the bone marrow, as well as in the form of hemosiderin in the skin, liver, pancreas, and myocardium, resulting in the development of secondary hemosiderosis. A general blood test will record anemia, erythropenia, and a decrease in color index.

Indicators of iron metabolism in the body are characterized by an increase in the concentration of ferritin and serum iron levels, normal indicators of life-saving blood test, and an increase in transferrin saturation with iron (in some cases reaching 100%). Thus, the main biochemical indicators that allow us to assess the state of iron metabolism in the body are ferritin, serum iron, total body mass and % transferrin saturation with iron.

Using indicators of iron metabolism in the body allows the clinician to:
- identify the presence and nature of iron metabolism disorders in the body;
- identify the presence of iron deficiency in the body at the preclinical stage;
- carry out differential diagnosis of hypochromic anemia;
- evaluate the effectiveness of the therapy.

Treatment of 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.

Iron deficiency anemia treatment program:
- eliminating the cause of iron deficiency anemia;
- therapeutic nutrition;
- ferrotherapy;
- prevention of relapses.

Patients with iron deficiency anemia are recommended to have a varied diet, including meat products (veal, liver) and products of plant origin (beans, soy, 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, and microelements, iron absorption of no more than 3-5 mg per day can be achieved. The use of iron supplements is necessary. Currently, the doctor has at his disposal a large arsenal of iron medications, characterized by different compositions 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 supplements, preference is given to drugs containing divalent 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 drug should have a minimum number of side effects, have a simple regimen of use, the best efficiency/price ratio, optimal iron content, and preferably the presence of factors that enhance absorption and stimulate hematopoiesis.

Indications for parenteral administration of iron preparations arise in case of intolerance to all oral drugs, malabsorption (ulcerative colitis, enteritis), gastric and duodenal ulcers during an exacerbation, with severe anemia and the vital need to quickly replenish iron deficiency. The effectiveness of iron supplements is judged by changes in laboratory parameters over time. By the 5-7th day of treatment, the number of reticulocytes increases by 1.5-2 times compared to the initial data. Starting from the 10th day of therapy, the hemoglobin content increases.

Considering the pro-oxidant and lysosomotropic effect of iron preparations, their parental administration can be combined with intravenous drip administration of rheopolyglucin (400 ml - once a week), which protects the cell and avoids iron overload of macrophages. Considering significant changes in the functional state of the erythrocyte membrane, activation of lipid peroxidation and a decrease in antioxidant protection of erythrocytes in iron deficiency anemia, it is necessary to introduce antioxidants, membrane stabilizers, cytoprotectors, antihypoxants into the treatment regimen, 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 used in the treatment of iron deficiency anemia:

Treatment of IDA includes treatment of the pathology that led to iron deficiency and the use of iron-containing drugs to restore iron reserves in the body. Identification and correction of pathological conditions that cause iron deficiency are the most important elements of complex treatment. Routine administration of iron-containing drugs to all patients with IDA is unacceptable, since it is not effective enough, is expensive and, more importantly, is often accompanied by diagnostic errors (non-detection of neoplasms).
The diet of patients with IDA should include meat products containing heme iron, which is absorbed better than from other products. It must be remembered that severe iron deficiency cannot be compensated for by diet alone.
Treatment of iron deficiency is carried out mainly with oral iron-containing drugs; parenteral drugs are used if there are special indications. It should be noted that the use of iron-containing oral medications is effective in most patients, whose body is able to absorb a sufficient amount of pharmacological iron to correct the deficiency. Currently, a large number of drugs containing iron salts are produced (ferroplex, orferon, tardiferon). The most convenient and cheapest are preparations containing 200 mg of ferrous sulfate, i.e. 50 mg of elemental iron in one tablet (ferrocal, ferroplex). The usual dose for adults is 1-2 tablets. 3 times a day. An adult patient should receive at least 3 mg of elemental iron per kg of body weight per day, i.e. 200 mg per day. The usual dosage for children is 2-3 mg of elemental iron per kg of body weight per day.
The effectiveness of preparations containing ferrous lactate, succinate or fumarate does not exceed the effectiveness of tablets containing ferrous sulfate or gluconate. The combination of iron salts and vitamins in one preparation, with the exception of the combination of iron and folic acid during pregnancy, as a rule, does not increase iron absorption. Although this effect can be achieved with large doses of ascorbic acid, the resulting adverse effects make therapeutic use of such a combination inappropriate. The effectiveness of slow-acting (retard) drugs is usually lower than that of conventional drugs because they enter the lower intestine, where iron is not absorbed, but it may be higher than that of fast-acting drugs taken with food.
It is not recommended to take a break of less than 6 hours between taking tablets, since for several hours after using the drug, duodenal enterocytes are refractory to iron absorption. Maximum absorption of iron occurs when taking the tablets on an empty stomach; taking it during or after meals reduces it by 50-60%. Do not take iron-containing medications with tea or coffee, which inhibit iron absorption.
Most adverse events when using iron-containing drugs are associated with gastrointestinal irritation. In this case, adverse events associated with irritation of the lower gastrointestinal tract (moderate constipation, diarrhea) usually do not depend on the dose of the drug, while the severity of irritation of the upper gastrointestinal tract (nausea, discomfort, pain in the epigastric region) is determined by the dose. Adverse effects are less common in children, although in them the use of iron-containing liquid mixtures may lead to temporary darkening of the teeth. To avoid this, you should give the drug to the root of the tongue, take the medicine with liquid and brush your teeth more often.
If there are severe side effects associated with irritation of the upper gastrointestinal tract, you can take the drug after meals or reduce the single dose. If adverse effects persist, you can prescribe drugs containing smaller amounts of iron, for example, in the composition of ferrous gluconate (37 mg of elemental iron per tablet). If in this case the adverse events do not stop, then you should switch to slow-acting drugs.
Improvement in the well-being of patients usually begins on the 4-6th day of adequate therapy, on the 10-11th day the number of reticulocytes increases, on the 16th-18th day the hemoglobin concentration begins to increase, microcytosis and hypochromia gradually disappear. The average rate of increase in hemoglobin concentration with adequate therapy is 20 g/l over 3 weeks. After 1-1.5 months of successful treatment with iron supplements, the dose can be reduced.
The main reasons for the lack of the expected effect when using iron-containing drugs are presented below. It should be emphasized that the main reason for the ineffectiveness of such treatment is ongoing bleeding, therefore identifying the source and stopping the bleeding is the key to successful therapy.
The main reasons for the ineffectiveness of treatment for iron deficiency anemia: ongoing blood loss; inappropriate use of medications:
- incorrect diagnosis (anemia in chronic diseases, thalassemia, sideroblastic anemia);
- combined deficiency (iron and vitamin B12 or folic acid);
- taking slow-acting medications containing iron: impaired absorption of iron supplements (rare).
It is important to remember that in order to restore iron reserves in the body in case of severe deficiency, the duration of taking iron-containing drugs should be at least 4-6 months or at least 3 months after normalization of hemoglobin levels in peripheral blood. The use of oral iron supplements does not lead to iron overload, since absorption is sharply reduced when iron stores are restored.
Prophylactic use of oral iron-containing drugs is indicated during pregnancy, patients receiving chronic hemodialysis, and blood donors. For premature babies, the use of nutritional mixtures containing iron salts is recommended.
Patients with IDA rarely need the use of parenteral drugs containing iron (ferrum-lek, imferon, ferkoven, etc.), since they usually respond quickly to treatment with oral drugs. Moreover, adequate therapy with oral medications, as a rule, is well tolerated even by patients with gastrointestinal pathology (peptic ulcer, enterocolitis, ulcerative colitis). The main indications for their use are the need to quickly compensate for iron deficiency (significant blood loss, upcoming surgery, etc.), severe side effects of oral medications, or impaired iron absorption due to damage to the small intestine. Parenteral administration of iron supplements may be accompanied by severe side effects and may also lead to excessive accumulation of iron in the body. Parenteral iron preparations do not differ from oral preparations in the rate of normalization of hematological parameters, although the rate of restoration of iron reserves in the body when using parenteral preparations is much higher. In any case, the use of parenteral iron supplements can be recommended only if the doctor is convinced that treatment with oral medications is ineffective or intolerable.
Iron preparations for parenteral use are usually administered intravenously or intramuscularly, with the intravenous route of administration being preferred. They contain from 20 to 50 mg of elemental iron per ml. The total dose of the drug is calculated using the formula:
Iron dose (mg) = (Hemoglobin deficiency (g/l)) / 1000 (Circulating blood volume) x 3.4.
The volume of circulating blood in adults is approximately 7% of body weight. To restore iron stores, 500 mg is usually added to the calculated dose. Before starting therapy, 0.5 ml of the drug is administered to exclude an anaphylactic reaction. If there are no signs of anaphylaxis within 1 hour, then the drug is administered so that the total dose is 100 mg. After this, 100 mg is administered daily until the total dose of the drug is reached. All injections are given slowly (1 ml per minute).
An alternative method involves simultaneous intravenous administration of the entire total dose of iron. The drug is dissolved in 0.9% sodium chloride solution so that its concentration is less than 5%. The infusion is started at a rate of 10 drops per minute; if there are no adverse events within 10 minutes, the rate of administration is increased so that the total duration of the infusion is 4-6 hours.
The most severe side effect of parenteral iron supplements is an anaphylactic reaction, which can occur with both intravenous and intramuscular administration. Although such reactions occur relatively rarely, the use of parenteral iron supplements should only be carried out in medical institutions that are fully equipped to provide emergency care. Other undesirable effects include facial flushing, increased body temperature, urticarial rash, arthralgia and myalgia, phlebitis (if the drug is administered too quickly). Drugs should not get under the skin. The use of parenteral iron supplements can lead to activation of rheumatoid arthritis.
Red blood cell transfusions are performed only in cases of severe IDA, accompanied by severe signs of circulatory failure, or upcoming surgical treatment.

Iron deficiency anemia B 12 is asymptomatic in most cases, but there are cases of sudden and acute progression of the disease. If a person feels weakness, irritation and rapid heartbeat for no reason, then it is necessary to seek medical help, since anemia code according to ICD 10, if left untreated, can lead to serious complications, including death.

Not many people know that a lack of substance in cells and muscles can lead to serious consequences. In particular, an insufficient amount of iron can lead to B 12 deficiency anemia, which is accompanied by symptoms such as impaired hemoglobinopoiesis and hypoxia of muscle tissue.

The main manifestations of the disease are general weakness, fatigue, drowsiness, and frequent dizziness. It can only be detected in laboratory conditions. To do this, you need to take a blood test, as well as study serum iron, ferrinite and TLC. Treatment of the disease is complex. But, first of all, the patient must make up for the deficiency of the element.

Diet is the most effective method of combating the disease. Drugs that replenish iron levels in the blood can only be prescribed by your doctor.

Symptoms of the disease

The clinical picture of anemia (ICD 10) is manifested by the following symptoms:

• frequent fainting;
• vomiting reflex;
• decreased mental and physical abilities, activity;
• extraneous noise in the ears;
• pale skin;
• increase/decrease in pressure.

Most often, it manifests itself differently in each person. One patient may not feel unwell, while another person may require urgent hospitalization. The degree of manifestations depends on the immune defense and individual characteristics of the person.

Treatment includes diet, taking medications containing iron, and transfusion of red blood cells. Only complex treatment can compensate for the microelement deficiency and improve the patient’s condition.

Distinctive features

In order to determine the presence of the disease, you need to know what anemia code is according to ICD 10. Microcytic disease is a consequence of a lack of a vital microelement - iron, which is involved in the synthesis of hemoglobin. The spread of the disease is determined by gender, age and climatic factors.

Statistics say that approximately 50% of newborns and infants, 15% of women aged 20 to 40 years, and 2% of men are susceptible to it. The disease is detected in every 3rd person worldwide. Various pathological conditions can lead to it, so identifying its source can be very difficult.

Iron is an essential element for the body. The level of oxygen that enters the cells depends on its quantity. In addition, without iron, redox processes, protection from toxins, infections, and normal functioning of the immune, endocrine, and nervous systems are impossible.

The normal level of iron is no more than 3-4 grams. Most of the element is found in hemoglobin, myoglobin, enzymes, the rest is in the liver, muscle tissue, bone marrow, heart and lungs. The need for iron is largely determined by a person’s age and gender.

Children who were born prematurely and adolescents need an increased dose of iron, as their body is in a phase of active growth and development. In addition, an increased amount of the element is necessary for women of reproductive age. During the menstrual cycle, a woman loses a large amount of blood, and therefore important microelements.

The most vulnerable categories of people who are predisposed to element deficiency include pregnant women and nursing mothers. Iron and its compounds are excreted from the body through sweat, urine, dead cells and feces. A person loses 1 mg of iron per day and replaces it in the amount of 2-2.5 mg. The element comes from food, drinks and vitamins taken.

Iron is absorbed better and faster if it enters the body with meat or liver, that is, with food of animal origin. Iron from plant products is practically not absorbed, or only a hundredth part of the element is absorbed. If the body does not adequately receive such a substance, then iron deficiency anemia develops.

Sources of anemia development

At 12, deficiency anemia can develop due to various mechanisms and factors that surround a person. In most cases, the disease develops with heavy blood loss. Iron-containing preparations and a complex of vitamins can cure the disease. In addition, a therapeutic diet is required, which includes meat products. Thus, B 12 deficiency anemia can be caused by:

• heavy periods;
• bleeding;
• anal fissures;
• helminthiasis;
• blood diseases;
• hemorrhoids.

Blood loss can occur due to injury and mechanical stress. Iron deficiency anemia is common in donors who donate blood frequently. B12 deficiency can be caused by disturbances in the absorption of iron into the gastrointestinal tract. Infections that occur in the intestines can cause a decrease in absorption. Diseases such as:

• gastritis;
• stomach ulcer;
• chronic enteritis;
• gastrectomy;
• malabsorption syndrome;
• anorexia.

If you limit yourself to eating meat products, then iron deficiency anemia develops, which is classified according to the ICD under code 10. In young children, the disease manifests itself if they are transferred to artificial feeding and the first complementary foods are introduced.

If a woman wants to lose weight, then the diet must be correct. If you limit your intake of food of animal origin, there may be serious consequences, including B 12 deficiency anemia.

Iron deficiency anemia B 12 can be caused by increased physical activity. Therefore, when playing sports, it is necessary to eat well and properly. Otherwise, the athlete may harm his health. In this case, not only iron deficiency anemia can develop, but also many other diseases.

Moreover, the disease develops if a person has cancer and viral infections. Therefore, a diet and complex therapy are needed that will compensate for the deficiency of iron and other microelements and improve immunity. During pregnancy and lactation, you need to take special vitamins and eat right.

Classification

Iron deficiency anemia due to lack of iron appears gradually. First of all, the prelatent form develops, which is accompanied by depletion of iron reserves. But at the same time, its normal transportation to the cells is observed. The second phase of the disease is latent deficiency. During this period, there is a sharp decrease in the amount of transported iron. Medicines can correct the situation.

There is a broad classification of the disease, which includes iron deficiency anemia, posthemorrhagic, and nutritional. If we classify the disease according to the degree of manifestation, then we distinguish anemia:

• light;
• moderate;
• heavy.

The disease can be detected using a blood test, since hemoglobin levels are determined in the laboratory. It is in it that a large amount of iron is concentrated, so this analysis is as accurate and effective as possible.

Anemia code according to ICD 10 most often occurs with virtually no symptoms and has no clinical manifestations. Therefore, patients turn to a medical institution when a severe form of iron deficiency develops - B 12, therefore urgent treatment, diet, and appropriate medications are necessary.

Diagnosis of the disease

There is an effective diagnosis of ICD 10 anemia by determining parameters, including:

• absence of anemia – normal hemoglobin level;
• decreased iron – signs of sideropenic syndrome;
• decreased serum iron;
• an increase in the total iron binding capacity of blood serum, which stands for the total ability of blood serum to bind iron.

This technique allows you to determine what stage of the disease is currently present. In addition, based on the following data, B 12 deficiency anemia can be diagnosed:

• a significant decrease in red blood cells and hemoglobin;
• reduced color index standards;
• the presence of hypochromia of erythrocytes, which is accompanied by the appearance of gaps in the center;
• anisocytosis, characterized by different cell sizes;
• increase in ESR.

Using a biochemical analysis, it is possible to determine whether there is a decrease in the level of serum iron and ferritin in the blood. But only a doctor can make an accurate diagnosis, since similar symptoms are characteristic of many other diseases. Therefore, it is necessary to monitor your health and, in case of any deviations, seek medical help. The sooner you visit a doctor, the more effective the treatment will be.

Many people treat code 10 anemia with folk remedies. But they can only be used after consulting a specialist, as they can cause an allergic reaction and other unpleasant consequences. Medicines prescribed for iron deficiency can relieve the disease in one course. Treatment usually lasts two weeks. During this time, the body can completely compensate for the deficiency of the microelement.

Before starting treatment, it is necessary to undergo a comprehensive examination. In this case, it is necessary not only to take tests, but also to examine the patient. If the diagnosis is confirmed, the patient should be provided with bed rest and drug therapy.