ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170
The release of a new revision (ICD-11) is planned by WHO in 2017-2018.
With changes and additions from WHO.
Processing and translation of changes © mkb-10.com
Iron deficiency anemia (ICD code D50)
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
Iron deficiency anemia ICD code D50
When treating iron deficiency anemia, the following medications are used:
The International Statistical Classification of Diseases and Related Health Problems is a document used as a leading framework in health care. ICD is normative document, ensuring the unity of methodological approaches and international comparability of materials. Currently in effect International classification diseases of the Tenth Revision (ICD-10, ICD-10). In Russia, health authorities and institutions transitioned statistical accounting to ICD-10 in 1999.
©g. ICD 10 - International Classification of Diseases, 10th Revision
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)
Excluded: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine diseases, nutritional and metabolic disorders (E00-E90), human immunodeficiency virus [HIV] disease (B20-B24), injury, poisoning and certain other effects of exposure external reasons(S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)
This class contains the following blocks:
D50-D53 Anemia associated with nutrition
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and hematopoietic organs
D80-D89 Selected disorders involving immune mechanism
The following categories are marked with an asterisk:
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere
NUTRITION-RELATED ANEMIA (D50-D53)
D50 Iron deficiency anemia
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified
D51 Vitamin B12 deficiency anemia
Excludes: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Congenital deficiency internal factor
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund(-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Anemia of vegetarians
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
D52 Folate deficiency anemia
D52.0 Folate deficiency anemia associated with nutrition. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia, drug-induced. If necessary, identify the drug
use an additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folate deficiency anemia, unspecified. Anemia caused by insufficient intake of folic acid, NOS
D53 Other diet-related anemias
Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folate
D53.0 Anemia due to protein deficiency. Anemia due to amino acid deficiency.
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: DiGuglielmo disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified anemias associated with nutrition.
Anemia associated with deficiency:
Excludes: malnutrition without mention of
anemia, such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Diet-related anemia, unspecified. Simple chronic anemia.
Excludes: anemia NOS (D64.9)
HEMOLYTIC ANEMIA (D55-D59)
D55 Anemia due to enzyme disorders
Excludes: drug-induced enzyme deficiency anemia (D59.2)
D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6-PD deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (except G-6-PD) associated with hexose monophosphate [HMP]
bypass of the metabolic pathway. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Hemolytic non-spherocytic (hereditary) type II
Due to hexokinase deficiency
Due to pyruvate kinase deficiency
Due to triosephosphate isomerase deficiency
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56 Thalassemia
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta thalassemia. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.
D56.3 Carriage of thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [HFH]
D56.9 Thalassemia, unspecified. Mediterranean anemia (with other hemoglobinopathy)
Thalassemia minor (mixed) (with other hemoglobinopathy)
D57 Sickle cell disorders
Excludes: other hemoglobinopathies (D58. -)
sickle cell beta thalassemia (D56.1)
D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
D57.2 Double heterozygous sickle cell disorders
D57.3 Carriage of the sickle cell trait. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders
D58 Other hereditary hemolytic anemias
D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
D58.8 Other specified hereditary hemolytic anemias. Stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59 Acquired hemolytic anemia
D59.0 Drug-induced autoimmune hemolytic anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease(cold type) (thermal type). Chronic disease caused by cold hemagglutinins.
Cold type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified. Chronic idiopathic hemolytic anemia
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 aplasias
D60.9 Acquired pure red cell aplasia, unspecified
D61 Other aplastic anemias
Excluded: agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) red cell:
Blackfan-Diamond syndrome. Familial hypoplastic anemia. Fanconi anemia. Pancytopenia with developmental defects
D61.1 Drug-induced aplastic anemia. If necessary, identify the drug
use an additional code for external causes (class XX).
D61.2 Aplastic anemia caused by other external agents.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D61.3 Idiopathic aplastic anemia
D61.8 Other specified aplastic anemias
D61.9 Aplastic anemia, unspecified. Hypoplastic anemia NOS. Hypoplasia bone marrow. Panmyelophthisis
D62 Acute posthemorrhagic anemia
Excludes: congenital anemia due to fetal blood loss (P61.3)
D63 Anemia in chronic diseases classified elsewhere
D63.0 Anemia due to neoplasms (C00-D48+)
D63.8 Anemia in others chronic diseases, classified in other headings
D64 Other anemias
Excluded: refractory anemia:
With excess blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
No sideroblasts (D46.0)
D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, an additional code is used to identify the disease.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshematopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
DiGuglielmo disease (C94.0)
D64.8 Other specified anemias. Childhood pseudoleukemia. Leukoerythroblastic anemia
BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS
HEMORRHAGIC CONDITIONS (D65-D69)
D65 Disseminated intravascular coagulation [defibration syndrome]
Afibrinogenemia acquired. Consumptive coagulopathy
Diffuse or disseminated intravascular coagulation
Acquired fibrinolytic bleeding
Excluded: defibration syndrome (complicating):
In a newborn (P60)
D66 Hereditary factor VIII deficiency
Factor VIII deficiency (with functional impairment)
Excluded: factor VIII deficiency c vascular disorder(D68.0)
D67 Hereditary factor IX deficiency
Factor IX (with functional impairment)
Thromboplastic plasma component
D68 Other bleeding disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and postpartum period(O45.0, O46.0, O67.0, O72.3)
D68.0 Von Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular impairment. Vascular hemophilia.
Excludes: hereditary capillary fragility (D69.8)
factor VIII deficiency:
With functional impairment (D66)
D68.1 Hereditary factor XI deficiency. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders caused by anticoagulants circulating in the blood. Hyperheparinemia.
If necessary, identify the anticoagulant used, use an additional external cause code.
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
Vitamin K deficiency
Excludes: vitamin K deficiency in the newborn (P53)
D68.8 Other specified bleeding disorders. Presence of systemic lupus erythematosus inhibitor
D68.9 Coagulation disorder, unspecified
D69 Purpura and other hemorrhagic conditions
Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
lightning purple (D65)
thrombotic thrombocytopenic purpura (M31.1)
D69.0 Allergic purpura.
D69.1 Qualitative platelet defects. Bernard-Soulier syndrome [giant platelets].
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). Thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excluded: thrombocytopenia with absence radius(Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified
OTHER DISEASES OF THE BLOOD AND BLOOD FORMING ORGANS (D70-D77)
D70 Agranulocytosis
Agranulocytic tonsillitis. Children's genetic agranulocytosis. Kostmann's disease
If it is necessary to identify the drug causing the neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)
D71 Functional disorders of polymorphonuclear neutrophils
Defect of the cell membrane receptor complex. Chronic (children's) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other white blood cell disorders
Excludes: basophilia (D75.8)
immune disorders (D80-D89)
preleukemia (syndrome) (D46.9)
D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
Excluded: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.8 Other specified white blood cell disorders.
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). Plasmacytosis
D72.9 White blood cell disorder, unspecified
D73 Diseases of the spleen
D73.0 Hyposplenism. Postoperative asplenia. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.5 Splenic infarction. Splenic rupture is non-traumatic. Torsion of the spleen.
Excludes: traumatic splenic rupture (S36.0)
D73.8 Other diseases of the spleen. Splenic fibrosis NOS. Perisplenitis. Splenitis NOS
D73.9 Disease of the spleen, unspecified
D74 Methemoglobinemia
D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified
D75 Other diseases of the blood and hematopoietic organs
Excludes: swollen lymph nodes (R59. -)
hypergammaglobulinemia NOS (D89.2)
Mesenteric (acute) (chronic) (I88.0)
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Decreased plasma volume
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs, unspecified
D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system
Excludes: Letterer-Sieve disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
Histiocytic medullary (C96.1)
D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schueller-Crisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If it is necessary to identify an infectious pathogen or disease, an additional code is used.
D76.3 Other histiocytosis syndromes. Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere.
Splenic fibrosis in schistosomiasis [bilharzia] (B65. -)
SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)
Includes: defects in the complement system, immunodeficiency disorders, excluding disease,
caused by human immunodeficiency virus [HIV] sarcoidosis
Excluded: autoimmune diseases(system) ODU (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)
D80 Immunodeficiencies with predominant antibody deficiency
D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Non-familial hypogammaglobulinemia. Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective deficiency of immunoglobulin G subclasses
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with increased content immunoglobulin M
D80.6 Antibody deficiency with immunoglobulin levels close to normal or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia of children
D80.8 Other immunodeficiencies with a predominant antibody defect. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified
D81 Combined immunodeficiencies
Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)
D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T- and B-cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell count
D81.3 Adenosine deaminase deficiency
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of the major histocompatibility complex
D81.8 Other combined immunodeficiencies. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency, unspecified. Severe combined immunodeficiency disorder NOS
D82 Immunodeficiencies associated with other significant defects
Excludes: ataxic telangiectasia [Louis-Bart] (G11.3)
D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di Georg syndrome. Pharyngeal diverticulum syndrome.
Aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified significant defects
D82.9 Immunodeficiency associated with significant defect, unspecified
D83 Common variable immunodeficiency
D83.0 General variable immunodeficiency with predominant abnormalities in the number and functional activity of B cells
D83.1 General variable immunodeficiency with a predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B- or T-cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified
D84 Other immunodeficiencies
D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. C1 esterase inhibitor deficiency
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified
D86 Sarcoidosis
D86.1 Sarcoidosis of lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.8 Sarcoidosis of other specified and combined localizations. Iridocyclitis in sarcoidosis (H22.1).
Multiple paralysis cranial nerves for sarcoidosis (G53.2)
Uveoparotitic fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified
D89 Other disorders involving the immune mechanism, not elsewhere classified
Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
non-engraftment and graft rejection (T86. -)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving the immune mechanism, unspecified. Immune disease NOS
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ICD code: D50
Iron-deficiency anemia
Iron-deficiency anemia
ICD code online / ICD code D50 / International Classification of Diseases / Diseases of the blood, hematopoietic organs and selected disorders involving the immune mechanism / Anemia associated with nutrition / Iron deficiency anemia
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ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170
The release of a new revision (ICD-11) is planned by WHO in 2017-2018.
With changes and additions from WHO.
Processing and translation of changes © mkb-10.com
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)
Excluded: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine diseases, nutritional and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), trauma, poisoning and certain other consequences of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)
This class contains the following blocks:
D50-D53 Anemia associated with nutrition
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and hematopoietic organs
D80-D89 Selected disorders involving the immune mechanism
The following categories are marked with an asterisk:
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere
NUTRITION-RELATED ANEMIA (D50-D53)
D50 Iron deficiency anemia
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified
D51 Vitamin B12 deficiency anemia
Excludes: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund(-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Anemia of vegetarians
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
D52 Folate deficiency anemia
D52.0 Folate deficiency anemia associated with nutrition. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia, drug-induced. If necessary, identify the drug
use an additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folate deficiency anemia, unspecified. Anemia due to insufficient intake of folic acid, NOS
D53 Other diet-related anemias
Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folate
D53.0 Anemia due to protein deficiency. Anemia due to amino acid deficiency.
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: DiGuglielmo disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified anemias associated with nutrition.
Anemia associated with deficiency:
Excludes: malnutrition without mention of
anemia, such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Diet-related anemia, unspecified. Simple chronic anemia.
Excludes: anemia NOS (D64.9)
HEMOLYTIC ANEMIA (D55-D59)
D55 Anemia due to enzyme disorders
Excludes: drug-induced enzyme deficiency anemia (D59.2)
D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6-PD deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (except G-6-PD) associated with hexose monophosphate [HMP]
bypass of the metabolic pathway. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Hemolytic non-spherocytic (hereditary) type II
Due to hexokinase deficiency
Due to pyruvate kinase deficiency
Due to triosephosphate isomerase deficiency
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56 Thalassemia
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta thalassemia. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.
D56.3 Carriage of thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [HFH]
D56.9 Thalassemia, unspecified. Mediterranean anemia (with other hemoglobinopathy)
Thalassemia minor (mixed) (with other hemoglobinopathy)
D57 Sickle cell disorders
Excludes: other hemoglobinopathies (D58. -)
sickle cell beta thalassemia (D56.1)
D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
D57.2 Double heterozygous sickle cell disorders
D57.3 Carriage of the sickle cell trait. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders
D58 Other hereditary hemolytic anemias
D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
D58.8 Other specified hereditary hemolytic anemias. Stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59 Acquired hemolytic anemia
D59.0 Drug-induced autoimmune hemolytic anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (warm type). Chronic disease caused by cold hemagglutinins.
Cold type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified. Chronic idiopathic hemolytic anemia
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 aplasias
D60.9 Acquired pure red cell aplasia, unspecified
D61 Other aplastic anemias
Excluded: agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) red cell:
Blackfan-Diamond syndrome. Familial hypoplastic anemia. Fanconi anemia. Pancytopenia with developmental defects
D61.1 Drug-induced aplastic anemia. If necessary, identify the drug
use an additional code for external causes (class XX).
D61.2 Aplastic anemia caused by other external agents.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D61.3 Idiopathic aplastic anemia
D61.8 Other specified aplastic anemias
D61.9 Aplastic anemia, unspecified. Hypoplastic anemia NOS. Bone marrow hypoplasia. Panmyelophthisis
D62 Acute posthemorrhagic anemia
Excludes: congenital anemia due to fetal blood loss (P61.3)
D63 Anemia in chronic diseases classified elsewhere
D63.0 Anemia due to neoplasms (C00-D48+)
D63.8 Anemia in other chronic diseases classified elsewhere
D64 Other anemias
Excluded: refractory anemia:
With excess blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
No sideroblasts (D46.0)
D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, an additional code is used to identify the disease.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshematopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
DiGuglielmo disease (C94.0)
D64.8 Other specified anemias. Childhood pseudoleukemia. Leukoerythroblastic anemia
BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS
HEMORRHAGIC CONDITIONS (D65-D69)
D65 Disseminated intravascular coagulation [defibration syndrome]
Afibrinogenemia acquired. Consumptive coagulopathy
Diffuse or disseminated intravascular coagulation
Acquired fibrinolytic bleeding
Excluded: defibration syndrome (complicating):
In a newborn (P60)
D66 Hereditary factor VIII deficiency
Factor VIII deficiency (with functional impairment)
Excludes: factor VIII deficiency with vascular disorder (D68.0)
D67 Hereditary factor IX deficiency
Factor IX (with functional impairment)
Thromboplastic plasma component
D68 Other bleeding disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and the puerperium (O45.0, O46.0, O67.0, O72.3)
D68.0 Von Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular impairment. Vascular hemophilia.
Excludes: hereditary capillary fragility (D69.8)
factor VIII deficiency:
With functional impairment (D66)
D68.1 Hereditary factor XI deficiency. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders caused by anticoagulants circulating in the blood. Hyperheparinemia.
If necessary, identify the anticoagulant used, use an additional external cause code.
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
Vitamin K deficiency
Excludes: vitamin K deficiency in the newborn (P53)
D68.8 Other specified bleeding disorders. Presence of systemic lupus erythematosus inhibitor
D68.9 Coagulation disorder, unspecified
D69 Purpura and other hemorrhagic conditions
Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
lightning purple (D65)
thrombotic thrombocytopenic purpura (M31.1)
D69.0 Allergic purpura.
D69.1 Qualitative platelet defects. Bernard-Soulier syndrome [giant platelets].
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). Thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excludes: thrombocytopenia with absent radius (Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified
OTHER DISEASES OF THE BLOOD AND BLOOD FORMING ORGANS (D70-D77)
D70 Agranulocytosis
Agranulocytic tonsillitis. Children's genetic agranulocytosis. Kostmann's disease
If it is necessary to identify the drug causing the neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)
D71 Functional disorders of polymorphonuclear neutrophils
Defect of the cell membrane receptor complex. Chronic (children's) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other white blood cell disorders
Excludes: basophilia (D75.8)
immune disorders (D80-D89)
preleukemia (syndrome) (D46.9)
D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
Excluded: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.8 Other specified white blood cell disorders.
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). Plasmacytosis
D72.9 White blood cell disorder, unspecified
D73 Diseases of the spleen
D73.0 Hyposplenism. Postoperative asplenia. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.5 Splenic infarction. Splenic rupture is non-traumatic. Torsion of the spleen.
Excludes: traumatic splenic rupture (S36.0)
D73.8 Other diseases of the spleen. Splenic fibrosis NOS. Perisplenitis. Splenitis NOS
D73.9 Disease of the spleen, unspecified
D74 Methemoglobinemia
D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified
D75 Other diseases of the blood and hematopoietic organs
Excludes: swollen lymph nodes (R59. -)
hypergammaglobulinemia NOS (D89.2)
Mesenteric (acute) (chronic) (I88.0)
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Decreased plasma volume
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs, unspecified
D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system
Excludes: Letterer-Sieve disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
Histiocytic medullary (C96.1)
D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schueller-Crisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If it is necessary to identify an infectious pathogen or disease, an additional code is used.
D76.3 Other histiocytosis syndromes. Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere.
Splenic fibrosis in schistosomiasis [bilharzia] (B65. -)
SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)
Includes: defects in the complement system, immunodeficiency disorders, excluding disease,
caused by human immunodeficiency virus [HIV] sarcoidosis
Excludes: autoimmune diseases (systemic) NOS (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)
D80 Immunodeficiencies with predominant antibody deficiency
D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Non-familial hypogammaglobulinemia. Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective deficiency of immunoglobulin G subclasses
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with increased levels of immunoglobulin M
D80.6 Antibody deficiency with immunoglobulin levels close to normal or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia of children
D80.8 Other immunodeficiencies with a predominant antibody defect. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified
D81 Combined immunodeficiencies
Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)
D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T- and B-cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell count
D81.3 Adenosine deaminase deficiency
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of the major histocompatibility complex
D81.8 Other combined immunodeficiencies. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency, unspecified. Severe combined immunodeficiency disorder NOS
D82 Immunodeficiencies associated with other significant defects
Excludes: ataxic telangiectasia [Louis-Bart] (G11.3)
D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di Georg syndrome. Pharyngeal diverticulum syndrome.
Aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified significant defects
D82.9 Immunodeficiency associated with significant defect, unspecified
D83 Common variable immunodeficiency
D83.0 General variable immunodeficiency with predominant abnormalities in the number and functional activity of B cells
D83.1 General variable immunodeficiency with a predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B- or T-cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified
D84 Other immunodeficiencies
D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. C1 esterase inhibitor deficiency
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified
D86 Sarcoidosis
D86.1 Sarcoidosis of lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.8 Sarcoidosis of other specified and combined localizations. Iridocyclitis in sarcoidosis (H22.1).
Multiple cranial nerve palsies in sarcoidosis (G53.2)
Uveoparotitic fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified
D89 Other disorders involving the immune mechanism, not elsewhere classified
Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
non-engraftment and graft rejection (T86. -)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving the immune mechanism, unspecified. Immune disease NOS
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ICD code: D50
Iron-deficiency anemia
Iron-deficiency anemia
ICD code online / ICD code D50 / International Classification of Diseases / Diseases of the blood, hematopoietic organs and selected disorders involving the immune mechanism / Anemia associated with nutrition / Iron deficiency anemia
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Among various anemic conditions iron deficiency anemia are the most common and account for about 80% of all anemias.
Iron-deficiency anemia- hypochromic microcytic anemia, which develops as a result of an absolute decrease in iron reserves in the body. Iron deficiency anemia occurs, as a rule, with chronic blood loss or insufficient intake of iron into the body.
According to the World Health Organization, every 3rd woman and every 6th man in the world (200 million people) suffer from iron deficiency anemia.
Iron metabolism
Iron is an essential biometal that plays an important role in the functioning of cells in many body systems. Biological significance iron is determined by its ability to reversibly oxidize and reduce. This property ensures the participation of iron in the processes of tissue respiration. Iron makes up only 0.0065% of body weight. The body of a man weighing 70 kg contains approximately 3.5 g (50 mg/kg body weight) of iron. The iron content in the body of a woman weighing 60 kg is approximately 2.1 g (35 mg/kg body weight). Iron compounds have different structures, have functional activity characteristic only of them and play an important biological role. The most important iron-containing compounds include: hemoproteins, structural component 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 bound to transferrin).
There are two types of iron: heme and non-heme. Heme iron is part of hemoglobin. It is contained only in a small part of the diet (meat products), is well absorbed (20-30%), its absorption is practically not affected by other food components. Non-heme iron is found in free ionic form - ferrous (Fe II) or ferric iron (Fe III). Most of dietary iron - non-heme (found mainly in vegetables). The degree of its absorption is lower than that of heme and depends on a number of factors. Only divalent non-heme iron is absorbed from food. To “convert” ferric iron into divalent iron, a reducing agent is needed, the role of which in most cases is played by ascorbic acid (vitamin C). During absorption in the cells of the intestinal mucosa, ferrous iron Fe2+ is converted into oxide Fe3+ and binds to a special carrier protein - transferrin, which transports iron to hematopoietic tissues and sites of iron deposition.
Iron accumulation is carried out by the proteins ferritin and hemosiderin. If necessary, iron can be actively released from ferritin and used for erythropoiesis. Hemosiderin is a derivative of ferritin with more high content gland. Iron is released slowly from hemosiderin. Incipient (prelatent) iron deficiency can be determined by a reduced concentration of ferritin even before the depletion of iron reserves, while still remaining normal concentration iron and transferrin in blood serum.
What causes iron deficiency anemia:
The main etiopathogenetic factor of development iron deficiency anemia- iron deficiency. The most common causes iron deficiency conditions are:
1. iron loss due to chronic bleeding (the most common cause, reaching 80%):
- bleeding from gastrointestinal tract: peptic ulcer, erosive gastritis, varicose veins esophageal veins, colon diverticula, hookworm infestations, tumors, UC, hemorrhoids;
- long and heavy menstruation, endometriosis, fibroids;
-- macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis, polycystic kidney disease, kidney and bladder tumors;
- nosebleeds, pulmonary bleeding;
-- blood loss during hemodialysis;
-- uncontrolled donation;
2. insufficient absorption of iron:
-- resection of the small intestine;
- chronic enteritis;
- malabsorption syndrome;
-- intestinal amyloidosis;
3. increased need for iron:
-- intensive growth;
-- pregnancy;
- period of breastfeeding;
- playing sports;
4. insufficient intake of iron from food:
-- newborns;
-- Small children;
-- vegetarianism.
Pathogenesis (what happens?) during Iron deficiency anemia:
Pathogenetically, the development of iron deficiency can be divided into several stages:
1. prelatent iron deficiency (insufficient accumulation) - there is a decrease in ferritin levels and a decrease in iron content in the bone marrow, increased iron absorption;
2. latent iron deficiency (iron deficiency erythropoiesis) - serum iron is further reduced, transferrin concentration increases, and the content of sideroblasts in the bone marrow decreases;
3. severe iron deficiency = iron deficiency anemia - the concentration of hemoglobin, red blood cells and hematocrit further decreases.
Symptoms of Iron Deficiency Anemia:
During the period of hidden iron deficiency, many subjective complaints appear and Clinical signs, characteristic of iron deficiency anemia. Patients note general weakness, malaise, and decreased performance. Already during this period, there may be a perversion of taste, dryness and tingling of the tongue, difficulty swallowing with a feeling foreign body sore throat, palpitations, shortness of breath.
An objective examination of patients reveals “minor symptoms of iron deficiency”: atrophy of the tongue papillae, cheilitis, dry skin and hair, brittle nails, burning and itching of the vulva. All these signs of impaired trophism of epithelial tissues are associated with tissue sideropenia and hypoxia.
Patients with iron deficiency anemia report general weakness, fatigue, difficulty concentrating, sometimes drowsiness. Appear headache, dizziness. Severe anemia may cause fainting. These complaints, as a rule, do not depend on the degree of decrease in hemoglobin, but on the duration of the disease and the age of the patients.
Iron deficiency anemia is also characterized by changes in the skin, nails and hair. The skin is usually pale, sometimes with a slight greenish tint (chlorosis) and with an easy blush on the cheeks, it becomes dry, flabby, peels, and cracks easily form. Hair loses its shine, turns grey, thins, breaks easily, thins and turns gray early. Changes in nails are specific: they become thin, matte, flattened, easily peel and break, and striations appear. With pronounced changes, the nails acquire a concave, spoon-shaped shape (koilonychia). Patients with iron deficiency anemia experience muscle weakness, which is not observed in other types of anemia. It is classified as a manifestation of tissue sideropenia. Atrophic changes occur in mucous membranes alimentary canal, respiratory organs, 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 Perversions of smell and taste (pica chlorotica) are observed: eating chalk, lime, raw cereals, pogophagia (craving for eating ice). Signs of tissue sideropenia quickly disappear after taking iron supplements.
Diagnosis of Iron Deficiency Anemia:
Basic landmarks in laboratory diagnostics iron deficiency anemia the following:
1. The average hemoglobin content in an erythrocyte in picograms (normal 27-35 pg) is reduced. To calculate it, the color index is multiplied by 33.3. For example, when color index 0.7 x 33.3 hemoglobin content is 23.3 pg.
2. The average concentration of hemoglobin in the erythrocyte is reduced; Normally it is 31-36 g/dl.
3. Hypochromia of erythrocytes is determined by smear microscopy peripheral blood and is characterized by an increase in the zone of central clearing in the erythrocyte; Normally, the ratio of central clearing to peripheral darkening is 1:1; for iron deficiency anemia - 2+3:1.
4. Microcytosis of erythrocytes - reduction in their size.
5. Coloring of erythrocytes of different intensity - anisochromia; the presence of both hypo- and normochromic red blood cells.
6. Different shape erythrocytes - poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and a period of ferrotherapy) in iron deficiency anemia remains normal.
8. The leukocyte count is also within normal limits (except in cases of blood loss or cancer pathology).
9. The platelet count often remains within normal limits; moderate thrombocytosis is possible with blood loss at the time of examination, and the platelet count decreases when the basis of iron deficiency anemia is blood loss due to thrombocytopenia (for example, with DIC syndrome, Werlhof's disease).
10. Reducing the number of siderocytes until they disappear (a siderocyte is an erythrocyte containing iron granules). In order to standardize the production of peripheral blood smears, it is recommended to use special automatic devices; the resulting monolayer of cells increases the quality of their identification.
Blood chemistry:
1. Decrease in iron content in blood serum (normally in men 13-30 µmol/l, in women 12-25 µmol/l).
2. The total life-value percentage is increased (reflects the amount of iron that can be bound due to free transferrin; the normal level of total life-value percentage is 30-86 µmol/l).
3. Study of transferrin receptors enzyme immunoassay method; their level is increased in patients with iron deficiency anemia (in patients with anemia chronic diseases- normal or reduced, despite similar indicators of iron metabolism.
4. The latent iron-binding capacity of the blood serum is increased (determined by subtracting the content indicator from the TBI indicators). serum iron).
5. The percentage of transferrin saturation with iron (the ratio of the serum iron index to the total life-saving value; normally 16-50%) is reduced.
6. The level of serum ferritin is also reduced (normally 15-150 mcg/l).
At the same time, in patients with iron deficiency anemia, the number of transferrin receptors is increased and the level of erythropoietin in the blood serum is increased (compensatory reactions of hematopoiesis). The volume of erythropoietin secretion is inversely proportional to the oxygen transport capacity of the blood and directly proportional to the oxygen demand of the blood. It should be taken into account that serum iron levels are higher in the morning; before and during menstruation it is higher than after menstruation. The iron content in blood serum in the first weeks of pregnancy is higher than in its last trimester. Serum iron levels increase 2-4 days after treatment 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 assessing the results of serum iron studies. It is equally important to follow the technique laboratory research, rules for blood sampling. Thus, the tubes in which blood is collected must first be washed with hydrochloric acid and double-distilled water.
Myelogram study reveals a moderate normoblastic reaction and a sharp decline content of sideroblasts (erythrokaryocytes containing iron granules).
Iron reserves in the body are judged by the results of the desferal test. In a healthy person, after intravenous administration of 500 mg of desferal, 0.8 to 1.2 mg of iron is excreted in the urine, while in a patient with iron deficiency anemia, iron excretion decreases to 0.2 mg. The new domestic drug defericolixam is identical to desferal, but circulates in the blood longer and therefore more accurately reflects the level of iron reserves in the body.
Taking into account the level of hemoglobin, iron deficiency anemia, like other forms of anemia, is divided into severe, moderate and mild degree. With mild iron deficiency anemia, the hemoglobin concentration is below normal, but more than 90 g/l; for iron deficiency anemia medium degree hemoglobin content is less than 90 g/l, but more than 70 g/l; with severe iron deficiency anemia, the hemoglobin concentration is less than 70 g/l. However, clinical signs of the severity of anemia (symptoms of a hypoxic nature) do not always correspond to the severity of anemia according to laboratory criteria. Therefore, a classification of anemia according to the severity of clinical symptoms has been proposed.
Based on clinical manifestations, there are 5 degrees of severity of anemia:
1. anemia without clinical manifestations;
2. moderate anemic syndrome;
3. severe anemic syndrome;
4. anemic precoma;
5. anemic coma.
Moderate severity of anemia is characterized general weakness, specific signs(for example, sideropenic or signs of vitamin B12 deficiency); with a pronounced degree of severity of anemia, palpitations, shortness of breath, dizziness, etc. appear. Precomatose and comatose states can develop in a matter of hours, which is especially typical for megaloblastic anemia.
Modern clinical researches show that laboratory and clinical heterogeneity is observed among patients with iron deficiency anemia. Thus, in some patients with signs of iron deficiency anemia and concomitant inflammatory and infectious diseases the level of serum and erythrocyte ferritin does not decrease, however, after the exacerbation of the underlying disease is eliminated, their content drops, which indicates the activation of macrophages in the processes of iron consumption. In some patients, the level of erythrocyte ferritin even increases, especially in patients with long-term iron deficiency anemia, which leads to ineffective erythropoiesis. Sometimes there is an increase in the level of serum iron and erythrocyte ferritin, a decrease in serum transferrin. It is assumed that in these cases the process of iron transfer to heme-synthesizing cells is disrupted. In some cases, a deficiency of iron, vitamin B12 and folic acid is simultaneously determined.
Thus, even the level of serum iron does not always reflect the degree of iron deficiency in the body in the presence of other signs of iron deficiency anemia. Only the level of THC in iron deficiency anemia is always elevated. Therefore, not one biochemical indicator, incl. OZHSS cannot be considered as absolute diagnostic criterion with iron deficiency anemia. At the same time, the morphological characteristics of peripheral blood erythrocytes and computer analysis of the main parameters of erythrocytes are decisive in the screening diagnosis of iron deficiency anemia.
Diagnosis of iron deficiency conditions is difficult in cases where the hemoglobin level remains normal. Iron deficiency anemia develops in the presence of the same risk factors as for iron deficiency anemia, as well as in persons with increased physiological need in the gland, especially in premature infants at an early age, in adolescents with a rapid increase in height and body weight, in blood donors, and with nutritional dystrophy. In the first stage of iron deficiency clinical manifestations are absent, and iron deficiency is determined by the content of hemosiderin in bone marrow macrophages and by the absorption of radioactive iron in the gastrointestinal tract. At the second stage (latent iron deficiency), an increase in the concentration of protoporphyrin in erythrocytes is observed, the number of sideroblasts decreases, and morphological characteristics(microcytosis, hypochromia of erythrocytes), the average content and concentration of hemoglobin in erythrocytes decreases, the level of serum and erythrocyte ferritin, and transferrin saturation with iron decrease. The hemoglobin level at this stage remains quite high, and clinical signs are characterized by a decrease in tolerance to physical activity. The third stage is manifested by obvious clinical and laboratory signs of anemia.
Examination of patients with iron deficiency anemia
To exclude anemia that has common features with iron deficiency anemia, and to identify the cause of iron deficiency, a complete clinical examination patient:
General blood analysis with the obligatory determination of the number of platelets, reticulocytes, and the study of erythrocyte morphology.
Blood chemistry: determination of the level of iron, TLC, ferritin, bilirubin (bound and free), hemoglobin.
In all cases it is necessary examine bone marrow aspirate before prescribing vitamin B12 (primarily for differential diagnosis with megaloblastic anemia).
To identify the cause of iron deficiency anemia in women, it is necessary to preliminary consultation a gynecologist to exclude diseases of the uterus and its appendages, and in men - an examination by a proctologist to exclude bleeding hemorrhoids and a urologist to exclude pathology of the prostate gland.
Known cases extragenital endometriosis, for example, in respiratory tract. In these cases, hemoptysis is observed; fiberoptic bronchoscopy with histological examination of a biopsy of the bronchial mucosa makes it possible to establish a diagnosis.
The examination plan also includes x-ray and endoscopic examination 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, X-ray and tomography of the lungs and sputum examination for alveolar macrophages containing hemosiderin are performed; in rare cases, histological examination of a lung biopsy is necessary. If kidney pathology is suspected, a general urine test, blood serum testing for urea and creatinine are required, and, if indicated, ultrasound and X-ray examination kidney In some cases, it is necessary to exclude endocrine pathology: myxedema, in which iron deficiency can develop secondary to iron deficiency small intestine; polymyalgia rheumatica - rare disease connective tissue in older women (less often in men), is characterized by pain in the muscles of the shoulder or pelvic girdle without any objective changes in them, and in a blood test - anemia and an increase in ESR.
Differential diagnosis of iron deficiency anemia
When diagnosing iron deficiency anemia, it is necessary to carry out differential diagnosis with other hypochromic anemias.
Iron redistribution anemia is a fairly common pathology and in terms of frequency of development it ranks second among all anemias (after iron deficiency anemia). It develops in acute and chronic infectious and inflammatory diseases, sepsis, tuberculosis, rheumatoid arthritis, liver diseases, oncological diseases, IHD, etc. Development mechanism hypochromic anemia in these conditions, it is associated with the redistribution of iron in the body (it is located mainly in the depot) and a violation of the mechanism for recycling iron from the depot. In the above diseases, activation of the macrophage system occurs, when macrophages, under activation conditions, firmly retain iron, thereby disrupting the process of its reutilization. IN general analysis blood there is a moderate decrease in hemoglobin (<80 г/л).
The main differences from iron deficiency anemia are:
- increased level of serum ferritin, which indicates an increased iron content in the depot;
- serum iron levels may remain within normal limits or be moderately reduced;
- TIHR remains within normal values or decreases, which indicates the absence of serum Fe starvation.
Iron-saturated anemia develops as a result of a violation of heme synthesis, which is caused by heredity or can be acquired. Heme is formed from protoporphyrin and iron in erythrokaryocytes. In iron-saturated anemia, the activity of enzymes involved in the synthesis of protoporphyrin occurs. The consequence of this is a violation of heme synthesis. Iron, which was not used for heme synthesis, is deposited in the form of ferritin in macrophages of the bone marrow, as well as in the form of hemosiderin in the skin, liver, pancreas, and myocardium, resulting in the development of secondary hemosiderosis. A general blood test will record anemia, erythropenia, and a decrease in color index.
Indicators of iron metabolism in the body are characterized by an increase in the concentration of ferritin and serum iron levels, normal indicators of life-saving blood test, and an increase in transferrin saturation with iron (in some cases reaching 100%). Thus, the main biochemical indicators that allow us to assess the state of iron metabolism in the body are ferritin, serum iron, total body mass and % transferrin saturation with iron.
Using indicators of iron metabolism in the body allows the clinician to:
- identify the presence and nature of iron metabolism disorders in the body;
- identify the presence of iron deficiency in the body at the preclinical stage;
- carry out differential diagnosis of hypochromic anemia;
- evaluate the effectiveness of the therapy.
Treatment of Iron Deficiency Anemia:
In all cases of iron deficiency anemia, it is necessary to establish the immediate cause of this condition and, if possible, eliminate it (most often, eliminate the source of blood loss or treat the underlying disease, complicated by sideropenia).
Treatment of iron deficiency anemia should be pathogenetically substantiated, comprehensive and aimed not only at eliminating anemia as a symptom, but also at eliminating iron deficiency and replenishing its reserves in the body.
Iron deficiency anemia treatment program:
- eliminating the cause of iron deficiency anemia;
- therapeutic nutrition;
- ferrotherapy;
- prevention of relapses.
Patients with iron deficiency anemia are recommended to have a varied diet, including meat products (veal, liver) and products of plant origin (beans, soy, parsley, peas, spinach, dried apricots, prunes, pomegranates, raisins, rice, buckwheat, bread). However, it is impossible to achieve an antianemic effect with diet alone. Even if the patient eats high-calorie foods containing animal protein, iron salts, vitamins, and microelements, iron absorption of no more than 3-5 mg per day can be achieved. The use of iron supplements is necessary. Currently, the doctor has at his disposal a large arsenal of iron medications, characterized by different compositions and properties, the amount of iron they contain, the presence of additional components that affect the pharmacokinetics of the drug, and various dosage forms.
According to the recommendations developed by WHO, when prescribing iron supplements, preference is given to drugs containing divalent iron. The daily dose should reach 2 mg/kg of elemental iron in adults. The total duration of treatment is at least three months (sometimes up to 4-6 months). An ideal iron-containing drug should have a minimum number of side effects, have a simple regimen of use, the best efficiency/price ratio, optimal iron content, and preferably the presence of factors that enhance absorption and stimulate hematopoiesis.
Indications for parenteral administration of iron preparations arise in case of intolerance to all oral drugs, malabsorption (ulcerative colitis, enteritis), gastric and duodenal ulcers during an exacerbation, with severe anemia and the vital need to quickly replenish iron deficiency. The effectiveness of iron supplements is judged by changes in laboratory parameters over time. By the 5-7th day of treatment, the number of reticulocytes increases by 1.5-2 times compared to the initial data. Starting from the 10th day of therapy, the hemoglobin content increases.
Considering the pro-oxidant and lysosomotropic effect of iron preparations, their parental administration can be combined with intravenous drip administration of rheopolyglucin (400 ml - once a week), which protects the cell and avoids iron overload of macrophages. Considering significant changes in the functional state of the erythrocyte membrane, activation of lipid peroxidation and a decrease in antioxidant protection of erythrocytes in iron deficiency anemia, it is necessary to introduce antioxidants, membrane stabilizers, cytoprotectors, antihypoxants into the treatment regimen, such as a-tocopherol up to 100-150 mg per day (or ascorutin, vitamin A, vitamin C, lipostabil, methionine, mildronate, etc.), and also combined with vitamins B1, B2, B6, B15, lipoic acid. In some cases, it is advisable to use ceruloplasmin.
List of drugs used in the treatment of iron deficiency anemia:
ICD 10. Class III. Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism (D50-D89)
Excluded: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine diseases, nutritional and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), trauma, poisoning and certain other consequences of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)
This class contains the following blocks:
D50-D53 Anemia associated with nutrition
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and hematopoietic organs
D80-D89 Selected disorders involving the immune mechanism
The following categories are marked with an asterisk:
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere
NUTRITION-RELATED ANEMIA (D50-D53)
D50 Iron deficiency anemia
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified
D51 Vitamin B12 deficiency anemia
Excludes: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund(-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Anemia of vegetarians
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
D52 Folate deficiency anemia
D52.0 Folate deficiency anemia associated with nutrition. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia, drug-induced. If necessary, identify the drug
use an additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folate deficiency anemia, unspecified. Anemia due to insufficient intake of folic acid, NOS
D53 Other diet-related anemias
Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folate
D53.0 Anemia due to protein deficiency. Anemia due to amino acid deficiency.
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: DiGuglielmo disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified anemias associated with nutrition.
Anemia associated with deficiency:
Excludes: malnutrition without mention of
anemia, such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Diet-related anemia, unspecified. Simple chronic anemia.
Excludes: anemia NOS (D64.9)
HEMOLYTIC ANEMIA (D55-D59)
D55 Anemia due to enzyme disorders
Excludes: drug-induced enzyme deficiency anemia (D59.2)
D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6-PD deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (except G-6-PD) associated with hexose monophosphate [HMP]
bypass of the metabolic pathway. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Hemolytic non-spherocytic (hereditary) type II
Due to hexokinase deficiency
Due to pyruvate kinase deficiency
Due to triosephosphate isomerase deficiency
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56 Thalassemia
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta thalassemia. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.
D56.3 Carriage of thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [HFH]
D56.9 Thalassemia, unspecified. Mediterranean anemia (with other hemoglobinopathy)
Thalassemia minor (mixed) (with other hemoglobinopathy)
D57 Sickle cell disorders
Excludes: other hemoglobinopathies (D58. -)
sickle cell beta thalassemia (D56.1)
D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
D57.2 Double heterozygous sickle cell disorders
D57.3 Carriage of the sickle cell trait. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders
D58 Other hereditary hemolytic anemias
D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
D58.8 Other specified hereditary hemolytic anemias. Stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59 Acquired hemolytic anemia
D59.0 Drug-induced autoimmune hemolytic anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (warm type). Chronic disease caused by cold hemagglutinins.
Cold type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified. Chronic idiopathic hemolytic anemia
D60 Acquired pure red cell aplasia (erythroblastopenia)
Includes: red cell aplasia (acquired) (adults) (with thymoma)
D60.0 Chronic acquired pure red cell aplasia
D60.1 Transient acquired pure red cell aplasia
D60.8 Other acquired pure red cell aplasias
D60.9 Acquired pure red cell aplasia, unspecified
D61 Other aplastic anemias
Excluded: agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) red cell:
Blackfan-Diamond syndrome. Familial hypoplastic anemia. Fanconi anemia. Pancytopenia with developmental defects
D61.1 Drug-induced aplastic anemia. If necessary, identify the drug
use an additional code for external causes (class XX).
D61.2 Aplastic anemia caused by other external agents.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D61.3 Idiopathic aplastic anemia
D61.8 Other specified aplastic anemias
D61.9 Aplastic anemia, unspecified. Hypoplastic anemia NOS. Bone marrow hypoplasia. Panmyelophthisis
D62 Acute posthemorrhagic anemia
Excludes: congenital anemia due to fetal blood loss (P61.3)
D63 Anemia in chronic diseases classified elsewhere
D63.0 Anemia due to neoplasms (C00-D48+)
D63.8 Anemia in other chronic diseases classified elsewhere
D64 Other anemias
With excess blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
No sideroblasts (D46.0)
D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, an additional code is used to identify the disease.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshematopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
DiGuglielmo disease (C94.0)
D64.8 Other specified anemias. Childhood pseudoleukemia. Leukoerythroblastic anemia
BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS
HEMORRHAGIC CONDITIONS (D65-D69)
D65 Disseminated intravascular coagulation [defibration syndrome]
Afibrinogenemia acquired. Consumptive coagulopathy
Diffuse or disseminated intravascular coagulation
Acquired fibrinolytic bleeding
Excluded: defibration syndrome (complicating):
In a newborn (P60)
D66 Hereditary factor VIII deficiency
Factor VIII deficiency (with functional impairment)
Excludes: factor VIII deficiency with vascular disorder (D68.0)
D67 Hereditary factor IX deficiency
Factor IX (with functional impairment)
Thromboplastic plasma component
D68 Other bleeding disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and the puerperium (O45.0, O46.0, O67.0, O72.3)
D68.0 Von Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular impairment. Vascular hemophilia.
Excludes: hereditary capillary fragility (D69.8)
factor VIII deficiency:
With functional impairment (D66)
D68.1 Hereditary factor XI deficiency. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders caused by anticoagulants circulating in the blood. Hyperheparinemia.
If necessary, identify the anticoagulant used, use an additional external cause code.
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
Vitamin K deficiency
Excludes: vitamin K deficiency in the newborn (P53)
D68.8 Other specified bleeding disorders. Presence of systemic lupus erythematosus inhibitor
D68.9 Coagulation disorder, unspecified
D69 Purpura and other hemorrhagic conditions
Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
lightning purple (D65)
thrombotic thrombocytopenic purpura (M31.1)
D69.0 Allergic purpura.
D69.1 Qualitative platelet defects. Bernard-Soulier syndrome [giant platelets].
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). Thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excludes: thrombocytopenia with absent radius (Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified
OTHER DISEASES OF THE BLOOD AND BLOOD FORMING ORGANS (D70-D77)
D70 Agranulocytosis
Agranulocytic tonsillitis. Children's genetic agranulocytosis. Kostmann's disease
If it is necessary to identify the drug causing the neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)
D71 Functional disorders of polymorphonuclear neutrophils
Defect of the cell membrane receptor complex. Chronic (children's) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other white blood cell disorders
Excludes: basophilia (D75.8)
immune disorders (D80-D89)
preleukemia (syndrome) (D46.9)
D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
Excluded: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.8 Other specified white blood cell disorders.
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). Plasmacytosis
D72.9 White blood cell disorder, unspecified
D73 Diseases of the spleen
D73.0 Hyposplenism. Postoperative asplenia. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.5 Splenic infarction. Splenic rupture is non-traumatic. Torsion of the spleen.
Excludes: traumatic splenic rupture (S36.0)
D73.8 Other diseases of the spleen. Splenic fibrosis NOS. Perisplenitis. Splenitis NOS
D73.9 Disease of the spleen, unspecified
D74 Methemoglobinemia
D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified
D75 Other diseases of the blood and hematopoietic organs
Excludes: swollen lymph nodes (R59. -)
hypergammaglobulinemia NOS (D89.2)
Mesenteric (acute) (chronic) (I88.0)
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Decreased plasma volume
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs, unspecified
D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system
Excludes: Letterer-Sieve disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
Histiocytic medullary (C96.1)
D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schueller-Crisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If it is necessary to identify an infectious pathogen or disease, an additional code is used.
D76.3 Other histiocytosis syndromes. Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere.
Splenic fibrosis in schistosomiasis [bilharzia] (B65. -)
SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)
Includes: defects in the complement system, immunodeficiency disorders, excluding disease,
caused by human immunodeficiency virus [HIV] sarcoidosis
Excludes: autoimmune diseases (systemic) NOS (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)
D80 Immunodeficiencies with predominant antibody deficiency
D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Non-familial hypogammaglobulinemia. Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective deficiency of immunoglobulin G subclasses
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with increased levels of immunoglobulin M
D80.6 Antibody deficiency with immunoglobulin levels close to normal or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia of children
D80.8 Other immunodeficiencies with a predominant antibody defect. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified
D81 Combined immunodeficiencies
Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)
D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T- and B-cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell count
D81.3 Adenosine deaminase deficiency
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of the major histocompatibility complex
D81.8 Other combined immunodeficiencies. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency, unspecified. Severe combined immunodeficiency disorder NOS
D82 Immunodeficiencies associated with other significant defects
Excludes: ataxic telangiectasia [Louis-Bart] (G11.3)
D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di Georg syndrome. Pharyngeal diverticulum syndrome.
Aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified significant defects
D82.9 Immunodeficiency associated with significant defect, unspecified
D83 Common variable immunodeficiency
D83.0 General variable immunodeficiency with predominant abnormalities in the number and functional activity of B cells
D83.1 General variable immunodeficiency with a predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B- or T-cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified
D84 Other immunodeficiencies
D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. C1 esterase inhibitor deficiency
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified
D86 Sarcoidosis
D86.1 Sarcoidosis of lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.8 Sarcoidosis of other specified and combined localizations. Iridocyclitis in sarcoidosis (H22.1).
Multiple cranial nerve palsies in sarcoidosis (G53.2)
Uveoparotitic fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified
D89 Other disorders involving the immune mechanism, not elsewhere classified
Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
non-engraftment and graft rejection (T86. -)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving the immune mechanism, unspecified. Immune disease NOS
APLASTIC AND OTHER ANEMIA (D60-D64)
Excluded: refractory anemia:
- NOS (D46.4)
- with excess blasts (D46.2)
- with transformation (C92.0)
- with sideroblasts (D46.1)
- without sideroblasts (D46.0)
In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170
The release of a new revision (ICD-11) is planned by WHO in 2017-2018.
With changes and additions from WHO.
Processing and translation of changes © mkb-10.com
Posthemorrhagic anemia
Posthemorrhagic anemia is a disease that is accompanied by a decrease in the number of red blood cells and hemoglobin concentration due to massive acute bleeding or as a result of even minor but chronic blood loss.
Hemoglobin is a protein complex of an erythrocyte that contains iron. Its main function is to transport oxygen through the bloodstream to all organs and tissues without exception. When this process is disrupted, quite serious changes begin in the body, which are determined by the etiology and severity of anemia.
Depending on the root cause and course of posthemorrhagic anemia, acute and chronic forms are distinguished. In accordance with the international classification system, the disease is divided as follows:
- Secondary iron deficiency anemia after blood loss. ICD 10 code D.50
- Acute posthemorrhagic anemia. ICD 10 code D.62.
- Congenital anemia after fetal bleeding – P61.3.
In clinical practice, secondary iron deficiency anemia is also called posthemorrhagic chronic anemia.
Causes of the acute form of the disease
The main reason for the development of acute posthemorrhagic anemia is the loss of a large volume of blood over a short period of time, which occurred as a result of:
- Trauma that caused damage to the main arteries.
- Damage to large blood vessels during surgery.
- Rupture of the fallopian tube during the development of an ectopic pregnancy.
- Diseases of the internal organs (most often the lungs, kidneys, heart, gastrointestinal tract), which can lead to acute massive internal bleeding.
In young children, the causes of acute posthemorrhagic anemia are most often umbilical cord injuries, congenital pathologies of the blood system, damage to the placenta during cesarean section, early placental abruption, placental previa, and birth trauma.
Causes of chronic posthemorrhagic anemia
Chronic posthemorrhagic anemia develops as a result of small but regular bleeding. They may appear as a result of:
- Hemorrhoids, which are accompanied by cracks in the rectum and the appearance of blood in the stool.
- Peptic ulcer of the stomach and duodenum.
- Heavy menstruation, uterine bleeding while taking hormonal medications.
- Damage to blood vessels by tumor cells.
- Chronic nosebleeds.
- Minor chronic blood loss in cancer.
- Frequent blood draws, catheter installations and other similar manipulations.
- Severe kidney disease with bleeding in the urine.
- Helminth infestation.
- Liver cirrhosis, chronic liver failure.
Chronic anemia of this etiology can also be caused by hemorrhagic diathesis. This is a group of diseases in which a person has a tendency to bleed due to disruption of homeostasis.
Symptoms and blood picture of anemia due to acute blood loss
The clinical picture of acute posthemorrhagic anemia develops very quickly. The main symptoms of this disease include manifestations of general shock as a result of acute bleeding. In general, the following are observed:
- Reduced blood pressure.
- Cloudiness or loss of consciousness.
- Severe pallor, bluish tint of the nasolabial fold.
- Thready pulse.
- Vomit.
- Increased sweating, and so-called cold sweat is observed.
- Chills.
- Cramps.
If the bleeding was successfully stopped, then such symptoms are replaced by dizziness, tinnitus, loss of orientation, blurred vision, shortness of breath, and irregular heartbeat. Pallor of the skin and mucous membranes and low blood pressure still persist.
Here you will find detailed information about treatment methods
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Changes in blood test results within a few days after bleeding has stopped and the development of anemia are closely related to compensation mechanisms that “turn on” in the body in response to the loss of a large volume of blood. They can be divided into the following stages:
- The reflex phase, which develops on the first day after blood loss. Redistribution and centralization of blood circulation begins, peripheral vascular resistance increases. In this case, a decrease in the number of red blood cells is observed at normal values of hemoglobin concentration and hematocrit.
- The hydremic phase occurs from the second to the fourth day. Extracellular fluid enters the vessels, glycogenolysis is activated in the liver, which leads to an increase in glucose content. Gradually, symptoms of anemia appear in the blood picture: the concentration of hemoglobin decreases, the hematocrit decreases. However, the color index value is still normal. Due to the activation of thrombus formation processes, the number of platelets decreases, and due to the loss of leukocytes during bleeding, leukopenia is observed.
- The bone marrow phase begins on the fifth day after bleeding. Insufficient oxygen supply to organs and tissues activates hematopoietic processes. In addition to decreased hemoglobin, hematocrit, thrombocytopenia and leukopenia, at this stage there is a decrease in the total number of red blood cells. When examining a blood smear, the presence of young forms of red blood cells is noted: reticulocytes, sometimes erythroblasts.
Similar changes in the blood picture are described in many situational tasks for future doctors.
Symptoms and diagnosis of anemia in chronic bleeding
Chronic posthemorrhagic anemia is similar in its symptoms to iron deficiency, since regular, mild bleeding leads to a deficiency of this microelement. The course of this blood disease depends on its severity. It is determined depending on the concentration of hemoglobin. Normally, in men it is 135–160 g/l, and in women 120–140 g/l. In children, this value varies depending on age from 200 in infants to 150 in adolescents.
Degree of posthemorrhagic chronic anemia Hemoglobin concentration
- 1 (light) degree 90 – 110 g/l
- 2nd degree (moderate) 70 – 90 g/l
- Grade 3 (severe) below 70 g/l
At the initial stage of development of the disease, patients complain of slight dizziness, flashing “spots” before the eyes, and increased fatigue. Externally, pallor of the skin and mucous membranes is noticeable.
At the second stage, the listed symptoms are added to a decrease in appetite, sometimes nausea, diarrhea or, conversely, constipation, shortness of breath. When listening to heart sounds, doctors note heart murmurs characteristic of chronic posthemorrhagic anemia. The condition of the skin also changes: the skin becomes dry and peels. Painful and inflamed cracks appear in the corners of the mouth. The condition of hair and nails worsens.
A severe degree of anemia is manifested by numbness and a tingling feeling in the fingers and toes, specific taste preferences appear, for example, some patients begin to eat chalk, and the perception of smells changes. Very often this stage of chronic posthemorrhagic anemia is accompanied by rapidly progressing caries and stomatitis.
Diagnosis of posthemorrhagic anemia is based on the results of a clinical blood test. In addition to the decrease in the amount of hemoglobin and red blood cells characteristic of all types of anemia, a decrease in the color index is detected. Its value ranges from 0.5 – 0.6. In addition, with chronic posthemorrhagic anemia, modified red blood cells (microcytes and schizocytes) appear.
Treatment of anemia after massive blood loss
First of all, it is necessary to stop the bleeding. If it is external, then it is necessary to apply a tourniquet and a pressure bandage and take the victim to the hospital. In addition to pallor, cyanosis and confusion, internal bleeding is indicated by severe dry mouth. It is impossible to help a person in this condition at home, so stopping internal bleeding is carried out only in a hospital setting.
After identifying the source and stopping the bleeding, it is urgently necessary to restore the blood supply to the vessels. For this purpose, rheopolyglucin, hemodez, polyglucin are prescribed. Acute blood loss is also compensated by blood transfusion, taking into account the compatibility of the Rh factor and blood group. The volume of blood transfusion is usually 400 – 500 ml. These measures must be carried out very quickly, since a rapid loss of even ¼ of the total blood volume can be fatal.
After stopping the state of shock and carrying out all the necessary manipulations, they proceed to standard treatment, which consists of the administration of iron supplements and enhanced nutrition to compensate for the deficiency of vitamins and microelements. Ferrum lek, ferlatum, maltofer are usually prescribed.
Typically, restoration of a normal blood picture occurs after 6–8 weeks, but the use of medications to normalize hematopoiesis continues for up to six months.
Treatment of chronic posthemorrhagic anemia
The first and most important step in the treatment of posthemorrhagic chronic anemia is to determine the source of bleeding and its elimination. Even the loss of 10 - 15 ml of blood per day deprives the body of the entire amount of iron that was received during that day with food.
A comprehensive examination of the patient is carried out, which necessarily includes consultations with a gastroenterologist, proctologist, hematologist, gynecologist for women, and endocrinologist. After identifying the disease that caused the development of chronic posthemorrhagic anemia, treatment begins immediately.
At the same time, medications that contain iron are prescribed. For adults, its daily dose is about 100 – 150 mg. Complex products are prescribed that, in addition to iron, contain ascorbic acid and B vitamins, which promote its better absorption. These are sorbifer durules, ferroplex, fenyuls.
In severe cases of posthemorrhagic chronic anemia, red blood cell transfusion and injection of drugs with iron are indicated to stimulate hematopoietic processes. Ferlatum, maltofer, likferr and similar medications are prescribed.
Recovery after the main course of treatment
The duration of taking iron-containing drugs is determined by the doctor. In addition to the use of various medications to restore normal oxygen supply to organs and replenish iron reserves in the body, proper nutrition is very important.
The diet of a person who has suffered posthemorrhagic anemia must contain proteins and iron. Preference should be given to meat, eggs, and dairy products. The leaders in iron content are meat by-products, especially beef liver, meat, fish, caviar, legumes, nuts, buckwheat and oatmeal.
When creating a diet, attention should be paid not only to how much iron a particular product contains, but also to the degree of its absorption in the body. It increases with the consumption of vegetables and fruits that contain vitamins B and C. These are citrus fruits, black currants, raspberries, etc.
Course and treatment of posthemorrhagic anemia in children
Posthemorrhagic anemia in children is much more severe, especially its acute form. The clinical picture of this pathology is practically no different from that of an adult, but develops faster. And if in an adult a certain volume of lost blood is compensated by the body’s protective reactions, then in a child this can lead to death.
Treatment of acute and chronic forms of posthemorrhagic anemia in children is the same. After identifying the cause and eliminating the bleeding, a transfusion of red blood cells is prescribed at the rate of 10 - 15 ml per kg of weight, and iron supplements. Their dosage is calculated individually depending on the severity of anemia and the condition of the child.
For children aged about six months, early introduction of complementary foods is recommended, and you should start with foods with a high iron content. Infants are advised to switch to special fortified formulas. If the disease that led to the development of posthemorrhagic anemia is chronic and cannot be treated, then preventive courses of iron supplements must be repeated regularly.
With timely initiation of treatment and non-critical blood loss, the prognosis is generally favorable. After compensation for iron deficiency, the child quickly recovers.
D50- D53- diet-related anemias:
D50 - iron deficiency;
D51 - vitamin B 12 – deficient;
D52 - folate deficiency;
D53 - other diet-related anemias.
D55- D59- hemolytic anemia:
D55- associated with enzymatic disorders;
D56 - thalassemia;
D57 - sickle cell;
D58 - other hereditary hemolytic anemias;
D59-acute acquired hemolytic.
D60- D64- aplastic and other anemias:
D60 - acquired red cell aplasia (erythroblastopenia);
D61-other aplastic anemia;
D62 - acute aplastic anemia;
D63-anemia of chronic diseases;
D64 - other anemias.
Pathogenesis
The supply of oxygen to tissues is provided by red blood cells - the formed elements of blood that do not contain a nucleus; the main volume of the red blood cell is occupied by hemoglobin - a protein that binds oxygen. The lifespan of red blood cells is about 100 days. When the hemoglobin concentration is below 100-120 g/l, oxygen delivery to the kidneys decreases, this stimulates the production of erythropoietin by the interstitial cells of the kidneys, which leads to the proliferation of erythroid cells of the bone marrow. For normal erythropoiesis it is necessary:
healthy bone marrow
healthy kidneys that produce 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 red blood cell formation. (T.R. Harrison).
Clinical picture
Clinical manifestations of anemia are determined by its severity, speed of development, and age of the patient. Under normal conditions, oxyhemoglobin releases only a small part of the oxygen associated with it to the tissues; the possibilities of this compensatory mechanism are great, and when Hb decreases 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.
When the Hb concentration is below 70-80 g/l, fatigue, shortness of breath during exercise, palpitations, and throbbing headaches appear.
In elderly patients with cardiovascular diseases, there is an increase in pain in the heart and an increase in signs of heart failure.
Acute blood loss leads to a rapid decrease in the number of red blood cells and blood volume. It is necessary, first of all, to assess the state of hemodynamics. Redistribution of blood flow and venous spasm cannot compensate for acute blood loss of more than 30%. Such patients lie down and have severe orthostatic hypotension and 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 sticky sweat, and decreased blood pressure. Emergency restoration of the central circulation is necessary.
In case of chronic bleeding, the blood volume has time to recover on its own, and a compensatory increase in blood volume and cardiac output develops. As a result, an increased apical impulse, a high pulse appear, the pulse pressure increases, and due to the accelerated flow of blood through the valve, a systolic murmur is heard during auscultation.
Paleness of the skin and mucous membranes becomes noticeable when the Hb concentration decreases to 80-100 g/l. Jaundice can also be a sign of anemia. When examining a patient, attention is paid to the condition of the lymphatic system, the size of the spleen and liver is determined, ossalgia is detected (pain when pounding bones, especially the sternum), attention should be drawn to petechiae, ecchymoses and other signs of coagulation disorders or bleeding.
Severity of anemia(by Hb level):
slight decrease in Hb 90-120 g/l
average Hb 70-90 g/l
heavy Hb<70 г/л
extremely heavy Hb<40 г/л
When making a diagnosis of anemia, you need to answer the following questions:
Are there any signs of bleeding or has it already occurred?
Are there signs of excessive hemolysis?
Are there signs of suppression of bone marrow hematopoiesis?
Are there any signs of iron metabolism disorders?
Are there signs of vitamin B12 or folic acid deficiency?
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