D50 Iron deficiency anemia. Hypochromic anemia Anemia ICD code 10 in children

Treatment of IDA includes treatment of the pathology that led to iron deficiency, and the use of iron supplements to restore iron stores in the body. Identification and correction pathological conditions, which are the cause of iron deficiency, are the most important elements complex treatment. Routine administration of iron-containing preparations 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 iron in the composition of heme, which is absorbed better than from other products. It must be remembered that it is impossible to compensate for a pronounced iron deficiency only by prescribing a diet.
Treatment of iron deficiency is carried out mainly with oral iron-containing preparations, parenteral drugs are used in the presence of special indications. It should be noted that the use of iron-containing oral preparations is effective in most patients whose body is able to adsorb the amount of pharmacological iron sufficient to correct the deficiency. Currently released a large number of preparations containing iron salts (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. Per day, an adult patient should receive at least 3 mg of elemental iron per kg of body weight, 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 in one preparation of iron salt and vitamins, with the exception of the combination of iron and folic acid during pregnancy, as a rule, does not increase the absorption of iron. Although this effect can be achieved with high doses of ascorbic acid, the resulting adverse events make the therapeutic use of such a combination impractical. Slow-acting (retard) drugs are usually less effective than regular drugs because they enter the lower intestines where iron is not absorbed, but may be higher than fast-acting drugs. active drugs taken with food.
It is not recommended to take a break between taking pills for less than 6 hours, because within a few hours after taking the drug, enterocytes duodenum refractory to iron absorption. The maximum absorption of iron occurs when taking tablets on an empty stomach, taking during or after a meal reduces it by 50-60%. Do not take iron supplements with tea or coffee, which inhibit iron absorption.
Most of the adverse events associated with the use of iron-containing preparations are associated with irritation of the gastrointestinal tract. At the same time, 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 sections (nausea, discomfort, pain in the epigastric region) is determined by the dose. Adverse events are less common in children, although in them the use of iron-containing liquid mixtures can lead to temporary darkening of the teeth. To avoid this, you should give the drug to the root of the tongue, drink the medicine with liquid and brush your teeth more often.
In the presence of severe adverse events associated with irritation of the upper gastrointestinal tract, you can take the drug after meals or reduce the single dose. If adverse events persist, lower iron preparations may be given, such as those in ferrous gluconate (37 mg elemental iron per tablet). If, in this case, adverse effects are not stopped, then you should switch to slow-acting drugs.
Improving the well-being of patients usually begins on the 4th-6th day of adequate therapy, on the 10th-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 for 3 weeks. After 1-1.5 months of successful treatment with iron preparations, their dose can be reduced.
The main reasons for the lack of the expected effect when using iron-containing preparations are presented below. It should be emphasized that the main reason for the ineffectiveness of such treatment is ongoing bleeding, so identifying the source and stopping bleeding is the key to successful therapy.
The main reasons for the ineffectiveness of the treatment of iron deficiency anemia: ongoing blood loss; incorrect drug intake:
misdiagnosis (anemia chronic diseases, thalassemia, sideroblastic anemia);
- combined deficiency (iron and vitamin B12 or folic acid);
- taking slow-acting preparations containing iron: malabsorption of iron preparations (rare).
It is important to remember that in order to restore iron stores in the body with a pronounced deficiency, the duration of iron-containing preparations should be at least 4-6 months or at least 3 months after the normalization of hemoglobin in peripheral blood. The use of oral iron preparations does not lead to iron overload, since absorption decreases sharply when iron stores are restored.
Preventive use oral iron preparations are indicated during pregnancy, patients receiving permanent hemodialysis, and blood donors. Premature babies are shown the use of nutritional mixtures containing iron salts.
Patients with IDA rarely require the use of parenteral preparations containing iron (ferrum-lek, imferon, ferkoven, etc.), since they usually respond quickly to treatment with oral preparations. Moreover, adequate oral therapy is generally well tolerated even by patients with gastrointestinal pathology ( peptic ulcer, enterocolitis, ulcerative colitis). The main indications for their use are the need for rapid replacement of iron deficiency (significant blood loss, upcoming surgery, etc.), pronounced side effects of oral drugs, or impaired absorption of iron due to damage. small intestine. Parenteral administration of iron preparations can be accompanied by severe adverse events, as well as lead to excessive accumulation of iron in the body. Parenteral iron preparations do not differ from oral preparations in terms of the rate of normalization of hematological parameters, although the rate of restoration of iron stores in the body with the use of parenteral preparations is much higher. In any case, the use of parenteral iron preparations can only be recommended if the doctor is convinced of the ineffectiveness or intolerance of treatment with oral preparations.
Parenteral iron preparations are usually administered intravenously or intramuscularly, with the intravenous route of administration being preferred. They contain 20 to 50 mg of elemental iron per ml. The total dose of the drug is calculated by the formula:
Dose of iron (mg) = (Hemoglobin deficiency (g / l)) / 1000 (Volume of circulating blood) 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 within 1 hour there are no signs of anaphylaxis, then the drug is administered so that the total dose is 100 mg. After that, 100 mg is administered daily until the total dose of the drug is reached. All injections are given slowly (1 ml per minute).
Alternative Method consists in a single intravenous administration the 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, in the absence of adverse events within 10 minutes, the rate of administration is increased so that the total duration of the infusion is 4-6 hours.
most severe side effect parenteral iron preparations is an anaphylactic reaction that can occur both with intravenous and with intramuscular injection. Although such reactions occur relatively rarely, the use of parenteral iron preparations should be carried out only in medical institutions equipped to provide emergency care in full. Other adverse events include flushing of the face, fever, urticaria, arthralgia and myalgia, phlebitis (with too rapid administration of the drug). Drugs should not get under the skin. The use of parenteral iron preparations can lead to activation rheumatoid arthritis.
Red blood cell transfusions are carried out only in case of severe IDA, accompanied by severe signs of circulatory failure, or the upcoming surgical treatment.

Differential Diagnosis anemic syndromes is an important detail management of patients, since depending on the pathogenesis, approaches to treatment will differ.

So Iron-deficiency anemia according to ICD 10, it has the D50 code, which distinguishes it from other types of this syndrome.

Separate chronic IDA are pathologies associated with intense blood loss, that is, appearing as a result of hemorrhagic syndrome, and IDA of primary origin. The mechanism for the development of hypochromic anemia without blood loss is associated with a lack of iron intake into the body, with immune processes that block its conversion or pathologies due to which malabsorption occurs.

Hypochromic anemia is always accompanied by a lack of hemoglobin in red blood cells, which includes iron.

IDA features

The anemic syndrome does not give specific manifestations, therefore, the mechanism of its development: lack of elements, hematopoietic problems, pronounced breakdown of red blood cells - are determined in the laboratory. In ICD 10 iron deficiency anemia coded for D50, which suggests the following diagnostic criteria:

• decrease in the number of red blood cells;
• decline color indicator;
• decrease in the amount of hemoglobin;
• low serum iron (with refractory anemia, the indicator, on the contrary, increases significantly).

AT medical institutions individual treatment protocols are used this disease. However, the IDA code implies general principles therapy based on iron preparations.

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 findings on clinical and laboratory research, 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 medicine

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) (thermal 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 necessary, to identify the drug, use an additional code of 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 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 of the 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 postpartum period(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 cranial nerve palsies 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 International classification diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to apply 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. №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.
• Major damage blood vessels during a surgical intervention.
• Gap fallopian tube with 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 most common causes of acute posthemorrhagic anemia are injuries to the umbilical cord, congenital pathologies 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

Clinical picture 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

This video takes a detailed look at the normal mechanism.

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About Chapter 19.08.

Dr. Komarovsky will explain what are the causes of an

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Anemia is a condition that is observed in practical

Hemolytic anemia is an anemia that develops in

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Anemia or anemia is a decrease in the concentration of

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Iron-deficiency anemia. Symptoms, Signs and Methods �

Anemia is one of the most common causes dropped out

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 at normal values ​​of hemoglobin concentration and hematocrit.
• 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, flashing "flies" before the eyes, 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 of a clinical blood test. 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 carried out only in a hospital setting.

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.

Held comprehensive examination patient, which without fail includes consultations of 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 it daily dose is about 100 - 150 mg. Appointed complex means 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, fermented milk 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 form 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.

Hypochromic anemia includes several types of anemia in which red blood cells are poorly stained and therefore unable to carry a sufficiently large amount of oxygenated hemoglobin. All types are included in the list of hypochromic anemia, microcytic anemia code 10. Microcytic anemia most often occurs due to the lack of adequate iron stores in the blood. Treatment usually consists of replenishing iron stores.

Microcytic anemia is one of the many types of anemia that characteristics include the appearance of an excess of red blood cells. They are small (medically called microcytes), this is normocytic hypochromic anemia. The main measure in the blood count that shows us microcytic anemia is the MCV (Mean Blood Cell Volume). If it is microcytic anemia, the MCV limit is 80 fL (or less).

In the course of microcytic anemia, red blood cells are usually unpigmented (that is, paler). This is due to a deficiency of hemoglobin in the blood cells, measured using the MCHC parameter (mean hemoglobin per erythrocyte).

Hypochromic anemia in children is divided into:

• iron deficiency anemia (the most common cause of anemia in general, considered mild hypochromic anemia);
• thalassemia;
• sideroblastic anemia;
• anemia in chronic diseases (in some cases);
• lead poisoning;
• caused by pyridoxine deficiency.

Hypochromic iron deficiency anemia

Iron deficiency anemia most often occurs due to a lack of adequate iron stores in the blood. This element is necessary for the creation of new red blood cells, its deficiency causes the appearance of diseased red blood cells compared to their healthy counterparts. The disease affects both children and adults.

What is hypochromic anemia and what are its causes? Diagnosis of iron deficiency anemia requires, firstly, determining the cause of the increased demand for this element or a decrease in its reserves in the body. Typical causes of iron deficiency are:

2 blood loss(blood cells contain iron, and the loss of a large volume of blood leads to its deficiency. In women, the most common cause is heavy monthly bleeding; due to stomach ulcers, vascular malformations in gastrointestinal tract, polyps and colorectal cancer. Sometimes chronic mucositis and blood loss through the digestive tract is caused by overuse of non-steroidal anti-inflammatory drugs (eg, Aspirin or Ibuprofen).

3 Improper nutrition(Lack of intake of foods rich in absorbable iron - red meat, eggs, liver, green leafy plants - is often accompanied by the wrong composition of a vegetarian diet).

4 Iron absorption disorders(many diseases limit the ability of the intestines to absorb iron, such as celiac disease, inflammatory diseases intestines and stomach, as well as conditions after surgical operations with the removal of long sections of the small intestine).

5 Pregnancy(a state of increased demand for iron - during pregnancy, blood volume increases significantly, because the mother's body needs to supply oxygen and nutrients developing fetus - lack of iron can slow the growth of the fetus).

6 Intravascular hemolysis(under this name, there is excessive destruction of red blood cells in the circulatory system, which can be caused by many factors, such as bacterial toxins).

7 Hemoglobinuria(the abnormal presence of hemoglobin in the urine due to the breakdown of red blood cells, for example, may be accompanied by malaria).

Chronic hypochromic anemia

Diagnosis of microcytic anemia with iron deficiency should be complemented by the exclusion of other equally important causes of this disease.

one . Microcytic anemia can be caused by abnormalities in the structure of hemoglobin chains that occur during a genetic disease called thalassemia. Depending on the type of mutation, the picture of symptoms and the severity of the disease are different. In diagnosis, it is important to accurately collect a medical history to identify similar symptoms in relatives, basic blood tests and detailed molecular diagnostics, which identifies the mutation that caused the disease.

2 Sideroblastic anemia. This cause of microcytic anemia is poorly understood. It is known to create abnormal cells called sideroblasts. It can be congenital or lifelong (caused by certain medications or other diseases). It is diagnosed by a thorough analysis of the blood picture and the search for factors that cause it to occur.

Symptoms of microcytic anemia

The symptoms of microcytic anemia are very similar to other types of anemia. by the most characteristic symptoms diseases are pallor of the skin (due to a decrease in the content of oxygenated hemoglobin in the tissues), general fatigue, dizziness and weakness. Sometimes, when microcytic anemia continues for many years, the body adjusts to the disease and some symptoms disappear. The disease turns into a severe degree of hypochromic anemia. In severe cases, shortness of breath occurs due to the lack of oxygen in the tissues. Other symptoms of microcytic anemia (which may come or go):

• feeling of fear and feeling threatened;
• irritability;
• chest pain;
• constipation;
• excessive sleepiness;
• mouth ulcers;
• noise in ears;
• heart palpitations;
• hair loss;
• loss of consciousness or a feeling of impending unconsciousness;
• depression;
• apnea;
• involuntary muscle cramps;
• pale yellow skin;
• nausea;
• burning sensation in the abdomen;
• menstrual disorders (without a cycle);
• inflammation or infection of the surface of the tongue;
• inflammation of the corners of the mouth;
• weakness of appetite;
• difficulty swallowing;
• insomnia;
• restless leg syndrome.

Hypochromic anemia treatment and prognosis

Hypochromic anemia, after establishing the cause, requires causative or symptomatic drug treatment. The most common form, that is, iron deficiency anemia, is treated by supplementing the reserves of this element (for hypochromic anemia, diets and additional drugs prescribed by a doctor) and eliminate the cause of the disease. It is important not only to take medications, but also to eat foods rich in iron. Other conditions that cause hypochromic microcytic anemia require the use of other agents, usually under the supervision of a physician and hematologist.

If the cause of the disease can be identified and eliminated, the prognosis is good. In the case of hypochromic anemia associated, for example, with thalassemia or poisoning, the prognosis depends on the severity of the disease and promptly implemented preventive and therapeutic measures. In some cases, the disease cannot be cured.

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ICD-10 disease classes

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International Statistical Classification of Diseases and Related Health Problems.

Iron deficiency anemia (D50)

Inclusions: anemia:

• sideropenic
• hypochromic

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to apply 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. №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

ICD 10. Class III (D50-D89)

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 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 necessary, to identify the drug, use an additional code of 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 Idiopathic hemolytic anemia, chronic

APLASTIC AND OTHER ANEMIA (D60-D64)

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 of the 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

Excludes: refractory anemia:

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 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. 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.

Excl.: thrombocytopenia with absence of 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

Excl.: 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 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 cranial nerve palsies 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

ICD 10 coding for iron deficiency anemia

Differential diagnosis of anemic syndromes is an important detail of patient management, since approaches to treatment will differ depending on the pathogenesis.

Therefore, iron deficiency anemia according to ICD 10 has the D50 code, which distinguishes it from other types of this syndrome.

Separate chronic IDA are pathologies associated with intense blood loss, that is, appearing as a result of hemorrhagic syndrome, and IDA of primary origin. The mechanism for the development of hypochromic anemia without blood loss is associated with a lack of iron intake into the body, with immune processes that block its conversion or pathologies due to which malabsorption occurs.

Hypochromic anemia is always accompanied by a lack of hemoglobin in red blood cells, which includes iron.

IDA features

The anemic syndrome does not give specific manifestations, therefore, the mechanism of its development: lack of elements, hematopoietic problems, pronounced breakdown of red blood cells - are determined in the laboratory. In ICD 10, iron deficiency anemia is coded D50, which suggests the following diagnostic criteria:

• decrease in the number of red blood cells;
• decrease in color index;
• decrease in the amount of hemoglobin;
• low serum iron (with refractory anemia, the indicator, on the contrary, increases significantly).

In medical institutions, individual protocols for the treatment of this disease are used. However, the IDA code implies the general principles of therapy, which is based on iron preparations.

Classification of anemia by mcb-x

D51 - vitamin B 12 - deficient;

D53 - other nutritional anemias.

D55 - associated with enzymatic disorders;

D58 - other hereditary hemolytic anemias;

D59-acute acquired hemolytic.

D60 - acquired red cell aplasia (erythroblastopenia);

D61 - other aplastic anemias;

D62 - acute aplastic anemia;

D63-anemia of chronic diseases;

Pathogenesis

The supply of tissues with oxygen is provided by erythrocytes - blood cells that do not contain a nucleus, the main volume of an erythrocyte is occupied by hemoglobin - an oxygen-binding protein. The life span of erythrocytes is about 100 days. When the hemoglobin concentration is below / l, oxygen delivery to the kidneys decreases, this is a stimulus for the production of erythropoietin by the interstitial cells of the kidneys, this leads to the proliferation of cells of the erythroid germ of the bone marrow. For normal erythropoiesis, it is necessary:

healthy bone marrow

healthy kidneys producing enough erythropoietin

sufficient content of substrate elements necessary for hematopoiesis (primarily iron).

Violation of one of these conditions leads to the development of anemia.

Figure 1. Scheme of erythrocyte formation. (T..R. Harrison).

Clinical picture

Clinical manifestations of anemia are determined by its severity, the rate of development, and the age of the patient. Under normal conditions, oxyhemoglobin gives the tissues only a small part of the oxygen associated with it, the possibilities of this compensatory mechanism are great, and with a decrease in Hb by 20-30 g / l, the release of oxygen to the tissues increases and there may be no clinical manifestations of anemia, anemia is often detected by a random blood test.

At a concentration of Hb below 70-80 g / l, fatigue appears, shortness of breath with physical activity, heartbeat, headache pulsating character.

Elderly patients with cardiovascular disease show increased pain syndrome in the heart, an increase in signs of heart failure.

Acute blood loss leads to a rapid decrease in the number of red blood cells and BCC. It is necessary, first of all, to assess the state of hemodynamics. Redistribution of blood flow and spasm of the veins cannot compensate for acute blood loss of more than 30%. Such patients lie down, marked orthostatic hypotension, tachycardia. Loss of more than 40% of blood (2000 ml) leads to shock, the signs of which are tachypnea and tachycardia at rest, stupor, cold clammy sweat, and a decrease in blood pressure. An urgent restoration of the BCC is needed.

With chronic bleeding, the BCC has time to recover on its own, a compensatory increase in BCC and cardiac output develops. As a result, an increased apex beat, a high pulse, an increase in pulse pressure appear, due to the accelerated flow of blood through the valve, a systolic murmur is heard during auscultation.

The pallor of the skin and mucous membranes becomes noticeable with a decrease in the concentration of Hb dog / l. Jaundice can also be a sign of anemia. When examining a patient, attention is paid to the condition lymphatic system, determine the size of the spleen, liver, reveal ossalgia (soreness when the bones are beaten, especially the sternum), petechiae, ecchymosis and other signs of coagulation disorders or bleeding should attract attention.

Severity of anemia (according to Hb level):

slight decrease in Hbg/l

average Hbg/l

severe Hb<70 г/л

extremely severe Hb<40 г/л

When making a diagnosis of anemia, you need to answer the following questions:

Are there signs of bleeding or has it already taken place?

Are there signs of excessive hemolysis?

Are there signs of suppression of bone marrow hematopoiesis?

Are there signs of iron metabolism disorders?

Are there signs of vitamin B 12 or folic acid deficiency?

D50 Iron deficiency anemia

What is iron deficiency anemia

Among the various anemic conditions, iron deficiency anemia is the most common and accounts for about 80% of all anemias.

Iron deficiency anemia is a hypochromic microcytic anemia that 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 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 determined 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 (the most common cause, reaching 80%):

Bleeding from the gastrointestinal tract: peptic ulcer, erosive gastritis, esophageal varicose veins, colonic diverticula, hookworm invasions, tumors, UC, hemorrhoids;

Prolonged and heavy menstruation, endometriosis, fibroids;

Macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis, polycystic kidney disease, tumors of the kidneys and bladder;

Nose, pulmonary bleeding;

Blood loss during hemodialysis;

2. insufficient absorption of iron:

Resection of the small intestine;

3. increased need for iron:

The period of breastfeeding;

4. insufficient intake of iron from food:

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 appear. 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 of a 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:

The main guidelines in the laboratory diagnosis of iron deficiency anemia are as follows:

1. The average content of hemoglobin in an erythrocyte in picograms (normapg) 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 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 form of erythrocytes - poikilocytosis.

7. The number of reticulocytes (in the absence of blood loss and the period of ferrotherapy) with iron deficiency anemia remains normal.

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 mkmol/l, in women mkmol/l).

2. TIBC is elevated (reflects the amount of iron that can be bound by free transferrin; TIBC is normal kmol / l).

3. Study of transferrin receptors by enzyme immunoassay; 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 the blood serum is increased (determined by subtracting the serum iron content from the FIA ​​values).

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 (in normal kg / 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 of 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. It is equally important to observe the technique of laboratory research, the rules of blood sampling. Thus, the test tubes in which blood is collected must first be washed with hydrochloric acid and bidistilled water.

The study of the myelogram reveals a moderate normoblastic reaction and a sharp decrease in the content of sideroblasts (erythrokaryocytes 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 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 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 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.

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 studies show that laboratory and clinical heterogeneity is observed among patients with iron deficiency anemia. 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 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 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, not a single biochemical indicator, incl. TIA 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 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, especially in premature babies at an early age, in adolescents with a rapid increase in body height and 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), there is an increase in the concentration of protoporphyrin in erythrocytes, a decrease in the number of sideroblasts, morphological signs appear (microcytosis, hypochromia of erythrocytes), a decrease in the average content and concentration of hemoglobin in erythrocytes, a decrease in the level of serum and erythrocyte ferritin, 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 test with the obligatory determination of the number of platelets, reticulocytes, the study of the morphology of erythrocytes.

Biochemical blood test: determination of the level of iron, OZhSS, ferritin, bilirubin (bound and free), hemoglobin.

In all cases, it is necessary to examine the bone marrow punctate 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 prostate pathology.

There are cases of extragenital endometriosis, for example in the 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, a histological examination of a lung biopsy is necessary. If a kidney pathology is suspected, a general urinalysis, a blood serum test for urea and creatinine are necessary, and, according to indications, 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 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 the blood test - anemia and an increase in ESR.

Differential diagnosis of iron deficiency anemia

When making a diagnosis of iron deficiency anemia, it is necessary to make a 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 for the 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 violation mechanism for the recycling of iron 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. In the general blood test, a moderate decrease in hemoglobin is noted (<80 г/л).

The main differences from iron deficiency anemia are:

Elevated serum ferritin levels, indicating an increased iron content in the depot;

Serum iron levels 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 may 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 iron metabolism disorders in the body;

To identify the presence of iron deficiency in the body at the preclinical stage;

Conduct differential diagnosis of hypochromic anemia;

Assess 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;

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.

Taking into account 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 allows protecting the cell and avoiding overload of macrophages 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 domg 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.