Chronic iron deficiency anemia. Symptoms and treatment of anemia. Diagnosis of iron deficiency anemia
D50- D53- nutritional anemias:
D50 - iron deficiency;
D51 - vitamin B 12 - deficient;
D52 - folic acid deficiency;
D53 - other nutritional 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 anemias;
D62 - acute aplastic anemia;
D63-anemia of chronic diseases;
D64 - other anemias.
Pathogenesis
The supply of tissues with oxygen is provided by erythrocytes - blood cells that do not contain a nucleus, the main volume of an erythrocyte is occupied by hemoglobin - an oxygen-binding protein. The life span of erythrocytes is about 100 days. At a hemoglobin concentration below 100-120 g/l, oxygen delivery to the kidneys decreases, this is a stimulus for the production of erythropoietin by the interstitial cells of the kidneys, this leads to the proliferation of cells of the erythroid germ of the bone marrow. For normal erythropoiesis, it is necessary:
healthy bone marrow
healthy kidneys producing enough erythropoietin
sufficient content of substrate elements necessary for hematopoiesis (primarily iron).
Violation of one of these conditions leads to the development of anemia.
Figure 1. Scheme of erythrocyte formation. (T..R. Harrison).
Clinical picture
Clinical manifestations of anemia are determined by its severity, the rate of development, and the age of the patient. Under normal conditions, oxyhemoglobin gives the tissues only a small part of the oxygen associated with it, the possibilities of this compensatory mechanism are great, and with a decrease in Hb by 20-30 g / l, the release of oxygen to the tissues increases and clinical manifestations of anemia may not be, anemia is often detected by a random blood test.
At a concentration of Hb below 70-80 g / l, fatigue, shortness of breath during physical exertion, palpitations, and throbbing headache appear.
In elderly patients with cardiovascular diseases, there is an increase in pain in the heart, an increase in signs of heart failure.
Acute blood loss leads to a rapid decrease in the number of red blood cells and BCC. It is necessary, first of all, to assess the state of hemodynamics. Redistribution of blood flow and spasm of the veins cannot compensate for acute blood loss of more than 30%. Such patients lie down, marked orthostatic hypotension, tachycardia. Loss of more than 40% of blood (2000 ml) leads to shock, the signs of which are tachypnea and tachycardia at rest, stupor, cold clammy sweat, and a decrease in blood pressure. An urgent restoration of the BCC is needed.
With chronic bleeding, the BCC has time to recover on its own, a compensatory increase in BCC and cardiac output develops. As a result, an increased apex beat, a high pulse, an increase in pulse pressure appear, due to the accelerated flow of blood through the valve, a systolic murmur is heard during auscultation.
The pallor of the skin and mucous membranes becomes noticeable when the concentration of Hb decreases to 80-100 g/l. Jaundice can also be a sign of anemia. When examining a patient, attention is drawn to the state of the lymphatic system, the size of the spleen, liver is determined, ossalgia is detected (pain when bones are beaten, especially the sternum), petechiae, ecchymosis and other signs of coagulation disorders or bleeding should attract attention.
Severity of anemia(by Hb level):
slight decrease in Hb 90-120 g/l
average Hb 70-90 g/l
severe Hb<70 г/л
extremely severe Hb<40 г/л
When making a diagnosis of anemia, you need to answer the following questions:
Are there signs of bleeding or has it already taken place?
Are there signs of excessive hemolysis?
Are there signs of suppression of bone marrow hematopoiesis?
Are there signs of iron metabolism disorders?
Are there signs of vitamin B 12 or folic acid deficiency?
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
Processing and translation of changes © mkb-10.com
ICD 10. Class III (D50-D89)
ICD 10. Class III. Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism (D50-D89)
Excludes: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine, nutritional and metabolic disorders (E00-E90), human immunodeficiency virus [HIV] disease (B20-B24), injury, poisoning and certain other effects of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified (R00-R99)
This class contains the following blocks:
D50-D53 Dietary anemia
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Coagulation disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and blood-forming organs
D80-D89 Selected disorders involving the immune mechanism
The following categories are marked with an asterisk:
D77 Other disorders of the blood and blood-forming organs in diseases classified elsewhere
NUTRITIONAL ANEMIA (D50-D53)
D50 Iron deficiency anemia
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson Syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified
D51 Vitamin B12 deficiency anemia
Excludes: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund (-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Vegetarian anemia
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
D52 Folate deficiency anemia
D52.0 Dietary folic deficiency anemia. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia drug-induced. If necessary, identify the drug
use additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folic deficiency anemia, unspecified Anemia due to inadequate intake of folic acid, NOS
D53 Other nutritional anemias
Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folates
D53.0 Anemia due to protein deficiency. Anemia due to lack of amino acids.
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anaemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: Di Guglielmo's disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified nutritional anaemias
Anemia associated with deficiency:
Excludes: malnutrition without mention of
anemia such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Nutritional anemia, unspecified Simple chronic anemia.
Excludes: anemia NOS (D64.9)
HEMOLYTIC ANEMIA (D55-D59)
D55 Anemia due to enzyme disorders
Excludes: drug-induced enzyme deficiency anemia (D59.2)
D55.0 Anemia due to deficiency of glucose-6-phosphate dehydrogenase [G-6-PD]. Favism. G-6-PD-deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (with the exception of G-6-PD) associated with hexose monophosphate [HMP]
metabolic pathway shunt. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Hemolytic non-spherocytic (hereditary) type II
Due to hexokinase deficiency
Due to pyruvate kinase deficiency
Due to deficiency of triose phosphate isomerase
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56 Thalassemia
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta-thalassemia. Anemia Cooley. Severe beta thalassemia. Sickle cell beta thalassemia.
D56.3 Thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [NPPH]
D56.9 Thalassemia, unspecified Mediterranean anemia (with other hemoglobinopathies)
Thalassemia (minor) (mixed) (with other hemoglobinopathies)
D57 Sickle cell disorders
Excludes: other hemoglobinopathies (D58.-)
sickle cell beta thalassemia (D56.1)
D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
D57.2 Double heterozygous sickle cell disorders
D57.3 Sickle cell carrier. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders
D58 Other hereditary hemolytic anemias
D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
D58.8 Other specified hereditary hemolytic anemias stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59 Acquired hemolytic anemia
D59.0 Drug-induced autoimmune hemolytic anemia.
If necessary, to identify the medicinal product, use an additional external cause code (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (heat type). Chronic disease caused by cold hemagglutinins.
Cold type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of fetus and newborn (P55.-)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If necessary, to identify the drug, use an additional code of external causes (class XX).
D59.3 Hemolytic uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified Idiopathic hemolytic anemia, chronic
APLASTIC AND OTHER ANEMIA (D60-D64)
D60 Acquired pure red cell aplasia (erythroblastopenia)
Includes: red cell aplasia (acquired) (adults) (with thymoma)
D60.0 Chronic acquired pure red cell aplasia
D60.1 Transient acquired pure red cell aplasia
D60.8 Other acquired pure red cell aplasia
D60.9 Acquired pure red cell aplasia, unspecified
D61 Other aplastic anemias
Excludes: agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) red cell:
Blackfan-Diamond Syndrome. Familial hypoplastic anemia. Anemia Fanconi. Pancytopenia with malformations
D61.1 Drug-induced aplastic anemia. If necessary, identify the drug
use an additional external cause code (class XX).
D61.2 Aplastic anemia due to other external agents.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D61.3 Idiopathic aplastic anemia
D61.8 Other specified aplastic anemias
D61.9 Aplastic anemia, unspecified Hypoplastic anemia NOS. Hypoplasia of the bone marrow. Panmyeloftis
D62 Acute posthemorrhagic anemia
Excludes: congenital anemia due to fetal blood loss (P61.3)
D63 Anemia in chronic diseases classified elsewhere
D63.0 Anemia in neoplasms (C00-D48+)
D63.8 Anemia in other chronic diseases classified elsewhere
D64 Other anemias
Excludes: refractory anemia:
With an excess of blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
Without sideroblasts (D46.0)
D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, to identify the disease, use an additional code.
D64.2 Secondary sideroblastic anemia due to drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshemopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
di Guglielmo's disease (C94.0)
D64.8 Other specified anemias. Pediatric pseudoleukemia. Leukoerythroblastic anemia
BLOOD COAGULATION DISORDERS, PURPLE AND OTHERS
HEMORRHAGIC CONDITIONS (D65-D69)
D65 Disseminated intravascular coagulation [defibrination syndrome]
Afibrinogenemia acquired. Consumption coagulopathy
Diffuse or disseminated intravascular coagulation
Fibrinolytic bleeding acquired
Excludes: defibrination syndrome (complicating):
Newborn (P60)
D66 Hereditary factor VIII deficiency
Factor VIII deficiency (with functional impairment)
Excludes: factor VIII deficiency with vascular disorder (D68.0)
D67 Hereditary factor IX deficiency
Factor IX (with functional impairment)
Thromboplastic component of plasma
D68 Other bleeding disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and puerperium (O45.0, O46.0, O67.0, O72.3)
D68.0 Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular damage. Vascular hemophilia.
Excludes: fragility of capillaries hereditary (D69.8)
factor VIII deficiency:
With functional impairment (D66)
D68.1 Hereditary deficiency of factor XI. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders due to circulating anticoagulants in the blood. Hyperheparinemia.
If it is necessary to identify the anticoagulant used, use an additional external cause code.
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
Vitamin K deficiency
Excludes: vitamin K deficiency in newborn (P53)
D68.8 Other specified bleeding disorders Presence of an inhibitor of systemic lupus erythematosus
D68.9 Coagulation disorder, unspecified
D69 Purpura and other hemorrhagic conditions
Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
fulminant purpura (D65)
thrombotic thrombocytopenic purpura (M31.1)
D69.0 Allergic purpura.
D69.1 Qualitative defects in platelets. Bernard-Soulier [giant platelet] syndrome.
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excl.: thrombocytopenia with absence of radius (Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified haemorrhagic conditions Fragility of capillaries (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified
OTHER DISEASES OF THE BLOOD AND BLOOD-MAKE ORGANS (D70-D77)
D70 Agranulocytosis
Agranulocytic angina. Children's genetic agranulocytosis. Kostmann disease
If necessary, to identify the drug that caused neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)
D71 Functional disorders of polymorphonuclear neutrophils
Defect of the receptor complex of the cell membrane. Chronic (children's) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other white blood cell disorders
Excludes: basophilia (D75.8)
immune disorders (D80-D89)
preleukemia (syndrome) (D46.9)
D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
Excludes: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.8 Other specified disorders of white blood cells
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). plasmacytosis
D72.9 White blood cell disorder, unspecified
D73 Diseases of the spleen
D73.0 Hyposplenism. Asplenia postoperative. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.5 Infarction of the spleen. Rupture of the spleen is non-traumatic. Torsion of the spleen.
Excludes: traumatic rupture of spleen (S36.0)
D73.8 Other diseases of the spleen. Fibrosis of the spleen NOS. Perisplenit. Spell NOS
D73.9 Disease of spleen, unspecified
D74 Methemoglobinemia
D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemias Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified
D75 Other diseases of the blood and blood-forming organs
Excl.: swollen lymph nodes (R59.-)
hypergammaglobulinemia NOS (D89.2)
Mesenteric (acute) (chronic) (I88.0)
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Decreased plasma volume
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and blood-forming organs Basophilia
D75.9 Disorder of the blood and blood-forming organs, unspecified
D76 Certain diseases involving the lymphoreticular tissue and the reticulohistiocytic system
Excludes: Letterer-Siwe disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
Histiocytic medullary (C96.1)
D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schuller-Chrisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytosis from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If necessary, to identify an infectious agent or disease, use an additional code.
D76.3 Other histiocytic syndromes Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. xanthogranuloma
D77 Other disorders of the blood and blood-forming organs in diseases classified elsewhere.
Fibrosis of the spleen in schistosomiasis [bilharzia] (B65.-)
SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)
Includes: defects in the complement system, immunodeficiency disorders excluding disease,
human immunodeficiency virus [HIV] sarcoidosis
Excl.: autoimmune diseases (systemic) NOS (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)
D80 Immunodeficiencies with predominant antibody deficiency
D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton's] (with growth hormone deficiency)
D80.1 Non-familial hypogammaglobulinemia Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective immunoglobulin G subclass deficiency
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with elevated immunoglobulin M
D80.6 Insufficiency of antibodies with close to normal levels of immunoglobulins or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia of children
D80.8 Other immunodeficiencies with a predominant defect in antibodies. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified
D81 Combined immunodeficiencies
Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)
D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T and B cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell count
D81.3 Adenosine deaminase deficiency
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Major histocompatibility complex class I deficiency. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of major histocompatibility complex
D81.8 Other combined immunodeficiencies. Deficiency of biotin-dependent carboxylase
D81.9 Combined immunodeficiency, unspecified Severe combined immunodeficiency disorder NOS
D82 Immunodeficiencies associated with other significant defects
Excludes: atactic telangiectasia [Louis Bar] (G11.3)
D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di George's syndrome. Syndrome of the diverticulum of the pharynx.
Aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified major defects
D82.9 Immunodeficiency associated with major defect, unspecified
D83 Common variable immunodeficiency
D83.0 Common variable immunodeficiency with predominant abnormalities in the number and functional activity of B-cells
D83.1 Common variable immunodeficiency with predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B or T cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified
D84 Other immunodeficiencies
D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. Deficiency of C1 esterase inhibitor
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified
D86 Sarcoidosis
D86.1 Sarcoidosis of lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.8 Sarcoidosis of other specified and combined sites. Iridocyclitis in sarcoidosis (H22.1).
Multiple cranial nerve palsies in sarcoidosis (G53.2)
Uveoparotitis fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified
D89 Other disorders involving the immune mechanism, not elsewhere classified
Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
graft failure and rejection (T86.-)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving immune mechanism, unspecified Immune disease NOS
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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 certain disorders involving the immune mechanism / Diet-related anemia / Iron deficiency anemia
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ICD 10. Class III. Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism (D50-D89)
Excludes: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine, nutritional and metabolic disorders (E00-E90), human immunodeficiency virus [HIV] disease (B20-B24), injury, poisoning and certain other effects of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified (R00-R99)
This class contains the following blocks:
D50-D53 Dietary anemia
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Coagulation disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and blood-forming organs
D80-D89 Selected disorders involving the immune mechanism
The following categories are marked with an asterisk:
D77 Other disorders of the blood and blood-forming organs in diseases classified elsewhere
NUTRITIONAL ANEMIA (D50-D53)
D50 Iron deficiency anemia
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson Syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified
D51 Vitamin B12 deficiency anemia
Excludes: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund (-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Vegetarian anemia
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
D52 Folate deficiency anemia
D52.0 Dietary folic deficiency anemia. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia drug-induced. If necessary, identify the drug
use additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folic deficiency anemia, unspecified Anemia due to inadequate intake of folic acid, NOS
D53 Other nutritional anemias
Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folates
D53.0 Anemia due to protein deficiency. Anemia due to lack of amino acids.
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anaemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: Di Guglielmo's disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified nutritional anaemias
Anemia associated with deficiency:
Excludes: malnutrition without mention of
anemia such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Nutritional anemia, unspecified Simple chronic anemia.
Excludes: anemia NOS (D64.9)
HEMOLYTIC ANEMIA (D55-D59)
D55 Anemia due to enzyme disorders
Excludes: drug-induced enzyme deficiency anemia (D59.2)
D55.0 Anemia due to deficiency of glucose-6-phosphate dehydrogenase [G-6-PD]. Favism. G-6-PD-deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (with the exception of G-6-PD) associated with hexose monophosphate [HMP]
metabolic pathway shunt. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Hemolytic non-spherocytic (hereditary) type II
Due to hexokinase deficiency
Due to pyruvate kinase deficiency
Due to deficiency of triose phosphate isomerase
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56 Thalassemia
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta-thalassemia. Anemia Cooley. Severe beta thalassemia. Sickle cell beta thalassemia.
D56.3 Thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [NPPH]
D56.9 Thalassemia, unspecified Mediterranean anemia (with other hemoglobinopathies)
Thalassemia (minor) (mixed) (with other hemoglobinopathies)
D57 Sickle cell disorders
Excludes: other hemoglobinopathies (D58.-)
sickle cell beta thalassemia (D56.1)
D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
D57.2 Double heterozygous sickle cell disorders
D57.3 Sickle cell carrier. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders
D58 Other hereditary hemolytic anemias
D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
D58.8 Other specified hereditary hemolytic anemias stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59 Acquired hemolytic anemia
D59.0 Drug-induced autoimmune hemolytic anemia.
If necessary, to identify the medicinal product, use an additional external cause code (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (heat type). Chronic disease caused by cold hemagglutinins.
Cold type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of fetus and newborn (P55.-)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If necessary, to identify the drug, use an additional code of external causes (class XX).
D59.3 Hemolytic uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified Idiopathic hemolytic anemia, chronic
D60 Acquired pure red cell aplasia (erythroblastopenia)
Includes: red cell aplasia (acquired) (adults) (with thymoma)
D60.0 Chronic acquired pure red cell aplasia
D60.1 Transient acquired pure red cell aplasia
D60.8 Other acquired pure red cell aplasia
D60.9 Acquired pure red cell aplasia, unspecified
D61 Other aplastic anemias
Excludes: agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) red cell:
Blackfan-Diamond Syndrome. Familial hypoplastic anemia. Anemia Fanconi. Pancytopenia with malformations
D61.1 Drug-induced aplastic anemia. If necessary, identify the drug
use an additional external cause code (class XX).
D61.2 Aplastic anemia due to other external agents.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D61.3 Idiopathic aplastic anemia
D61.8 Other specified aplastic anemias
D61.9 Aplastic anemia, unspecified Hypoplastic anemia NOS. Hypoplasia of the bone marrow. Panmyeloftis
D62 Acute posthemorrhagic anemia
Excludes: congenital anemia due to fetal blood loss (P61.3)
D63 Anemia in chronic diseases classified elsewhere
D63.0 Anemia in neoplasms (C00-D48+)
D63.8 Anemia in other chronic diseases classified elsewhere
D64 Other anemias
With an excess of blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
Without sideroblasts (D46.0)
D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, to identify the disease, use an additional code.
D64.2 Secondary sideroblastic anemia due to drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshemopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
di Guglielmo's disease (C94.0)
D64.8 Other specified anemias. Pediatric pseudoleukemia. Leukoerythroblastic anemia
BLOOD COAGULATION DISORDERS, PURPLE AND OTHERS
HEMORRHAGIC CONDITIONS (D65-D69)
D65 Disseminated intravascular coagulation [defibrination syndrome]
Afibrinogenemia acquired. Consumption coagulopathy
Diffuse or disseminated intravascular coagulation
Fibrinolytic bleeding acquired
Excludes: defibrination syndrome (complicating):
Newborn (P60)
D66 Hereditary factor VIII deficiency
Factor VIII deficiency (with functional impairment)
Excludes: factor VIII deficiency with vascular disorder (D68.0)
D67 Hereditary factor IX deficiency
Factor IX (with functional impairment)
Thromboplastic component of plasma
D68 Other bleeding disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and puerperium (O45.0, O46.0, O67.0, O72.3)
D68.0 Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular damage. Vascular hemophilia.
Excludes: fragility of capillaries hereditary (D69.8)
factor VIII deficiency:
With functional impairment (D66)
D68.1 Hereditary deficiency of factor XI. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders due to circulating anticoagulants in the blood. Hyperheparinemia.
If it is necessary to identify the anticoagulant used, use an additional external cause code.
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
Vitamin K deficiency
Excludes: vitamin K deficiency in newborn (P53)
D68.8 Other specified bleeding disorders Presence of an inhibitor of systemic lupus erythematosus
D68.9 Coagulation disorder, unspecified
D69 Purpura and other hemorrhagic conditions
Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
fulminant purpura (D65)
thrombotic thrombocytopenic purpura (M31.1)
D69.0 Allergic purpura.
D69.1 Qualitative defects in platelets. Bernard-Soulier [giant platelet] syndrome.
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excl.: thrombocytopenia with absence of radius (Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified haemorrhagic conditions Fragility of capillaries (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified
OTHER DISEASES OF THE BLOOD AND BLOOD-MAKE ORGANS (D70-D77)
D70 Agranulocytosis
Agranulocytic angina. Children's genetic agranulocytosis. Kostmann disease
If necessary, to identify the drug that caused neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)
D71 Functional disorders of polymorphonuclear neutrophils
Defect of the receptor complex of the cell membrane. Chronic (children's) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other white blood cell disorders
Excludes: basophilia (D75.8)
immune disorders (D80-D89)
preleukemia (syndrome) (D46.9)
D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
Excludes: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.8 Other specified disorders of white blood cells
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). plasmacytosis
D72.9 White blood cell disorder, unspecified
D73 Diseases of the spleen
D73.0 Hyposplenism. Asplenia postoperative. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.5 Infarction of the spleen. Rupture of the spleen is non-traumatic. Torsion of the spleen.
Excludes: traumatic rupture of spleen (S36.0)
D73.8 Other diseases of the spleen. Fibrosis of the spleen NOS. Perisplenit. Spell NOS
D73.9 Disease of spleen, unspecified
D74 Methemoglobinemia
D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemias Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified
D75 Other diseases of the blood and blood-forming organs
Excl.: swollen lymph nodes (R59.-)
hypergammaglobulinemia NOS (D89.2)
Mesenteric (acute) (chronic) (I88.0)
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Decreased plasma volume
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and blood-forming organs Basophilia
D75.9 Disorder of the blood and blood-forming organs, unspecified
D76 Certain diseases involving the lymphoreticular tissue and the reticulohistiocytic system
Excludes: Letterer-Siwe disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
Histiocytic medullary (C96.1)
D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schuller-Chrisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytosis from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If necessary, to identify an infectious agent or disease, use an additional code.
D76.3 Other histiocytic syndromes Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. xanthogranuloma
D77 Other disorders of the blood and blood-forming organs in diseases classified elsewhere.
Fibrosis of the spleen in schistosomiasis [bilharzia] (B65.-)
SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)
Includes: defects in the complement system, immunodeficiency disorders excluding disease,
human immunodeficiency virus [HIV] sarcoidosis
Excl.: autoimmune diseases (systemic) NOS (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)
D80 Immunodeficiencies with predominant antibody deficiency
D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton's] (with growth hormone deficiency)
D80.1 Non-familial hypogammaglobulinemia Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective immunoglobulin G subclass deficiency
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with elevated immunoglobulin M
D80.6 Insufficiency of antibodies with close to normal levels of immunoglobulins or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia of children
D80.8 Other immunodeficiencies with a predominant defect in antibodies. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified
D81 Combined immunodeficiencies
Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)
D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T and B cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell count
D81.3 Adenosine deaminase deficiency
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Major histocompatibility complex class I deficiency. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of major histocompatibility complex
D81.8 Other combined immunodeficiencies. Deficiency of biotin-dependent carboxylase
D81.9 Combined immunodeficiency, unspecified Severe combined immunodeficiency disorder NOS
D82 Immunodeficiencies associated with other significant defects
Excludes: atactic telangiectasia [Louis Bar] (G11.3)
D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di George's syndrome. Syndrome of the diverticulum of the pharynx.
Aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified major defects
D82.9 Immunodeficiency associated with major defect, unspecified
D83 Common variable immunodeficiency
D83.0 Common variable immunodeficiency with predominant abnormalities in the number and functional activity of B-cells
D83.1 Common variable immunodeficiency with predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B or T cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified
D84 Other immunodeficiencies
D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. Deficiency of C1 esterase inhibitor
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified
D86 Sarcoidosis
D86.1 Sarcoidosis of lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.8 Sarcoidosis of other specified and combined sites. Iridocyclitis in sarcoidosis (H22.1).
Multiple cranial nerve palsies in sarcoidosis (G53.2)
Uveoparotitis fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified
D89 Other disorders involving the immune mechanism, not elsewhere classified
Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
graft failure and rejection (T86.-)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving immune mechanism, unspecified Immune disease NOS
APLASTIC AND OTHER ANEMIA (D60-D64)
Excludes: refractory anemia:
- NOS (D46.4)
- with excess blasts (D46.2)
- with transformation (C92.0)
- with sideroblasts (D46.1)
- without sideroblasts (D46.0)
In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to contact medical institutions of all departments, and causes of death.
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
Processing and translation of changes © mkb-10.com
Posthemorrhagic anemia
Posthemorrhagic anemia is a disease that is accompanied by a decrease in the number of red blood cells and hemoglobin concentration due to massive acute bleeding or as a result of even minor but chronic blood loss.
Hemoglobin is a protein complex of erythrocytes, which includes iron. Its main function is to carry oxygen with the blood flow to all organs and tissues without exception. If this process is disturbed, rather serious changes begin in the body, which are determined by the etiology and severity of anemia.
Depending on the underlying cause and course of posthemorrhagic anemia, acute and chronic forms are distinguished. In accordance with the international classification system, the disease is divided as follows:
- Secondary iron deficiency anemia after blood loss. ICD code 10 D.50
- Acute posthemorrhagic anemia. ICD code 10 D.62.
- Congenital anemia after hemorrhage in the fetus - P61.3.
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 trauma to the umbilical cord, congenital pathologies of the blood system, damage to the placenta during cesarean section, early abruption of the placenta, its presentation, and birth trauma.
Causes of the chronic course of posthemorrhagic anemia
Chronic posthemorrhagic anemia develops as a result of small but regular bleeding. They may appear as a result of:
- Hemorrhoids, which is accompanied by fissures of the rectum, the appearance of blood impurities in the feces.
- Peptic ulcer of the stomach and duodenum.
- Abundant menstruation, uterine bleeding while taking hormonal drugs.
- Vascular lesions by tumor cells.
- Chronic nosebleeds.
- Insignificant chronic blood loss in oncological diseases.
- Frequent blood sampling, catheter placement and other similar manipulations.
- Severe course of kidney disease with the release of blood in the urine.
- Helminth infestation.
- Cirrhosis of the liver, chronic liver failure.
The cause of chronic anemia of a similar etiology can also be hemorrhagic diathesis. This is a group of diseases in which a person has a tendency to bleed due to a violation of homeostasis.
Symptoms and picture of blood in anemia as a result of acute blood loss
The clinical picture of acute posthemorrhagic anemia develops very quickly. The main symptoms of this disease are accompanied by manifestations of general shock as a result of acute bleeding. In general, there are:
- Decreased blood pressure.
- Cloudiness or loss of consciousness.
- Strong pallor, bluish tint of the nasolabial fold.
- Thready pulse.
- Vomit.
- Excessive sweating, and there is a so-called cold sweat.
- Chills.
- Seizures.
If the bleeding has been successfully stopped, then such symptoms are replaced by dizziness, tinnitus, loss of orientation, blurred vision, shortness of breath, heart rhythm disturbances. The pallor of the skin and mucous membranes, low blood pressure is still preserved.
Here you will find detailed information about the treatment methods.
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Changes in the results of a blood test within a few days after stopping bleeding and the development of anemia are closely related to the compensation mechanisms that are “turned on” in the body in response to the loss of a large volume of blood. They can be divided into the following stages:
- The reflex phase, which develops on the first day after blood loss. Redistribution and centralization of blood circulation begins, peripheral vascular resistance increases. At the same time, a decrease in the number of erythrocytes is observed at normal values of hemoglobin concentration and hematocrit.
- The hydremic phase runs from the second to the fourth day. Extracellular fluid enters the vessels, glycogenolysis is activated in the liver, which leads to an increase in glucose content. Gradually, symptoms of anemia appear in the blood picture: the concentration of hemoglobin decreases, the hematocrit decreases. However, the value of the color index is still normal. Due to the activation of thrombus formation processes, the number of platelets decreases, and due to the loss of leukocytes during bleeding, leukopenia is observed.
- The bone marrow phase begins on the fifth day after bleeding. Insufficient supply of organs and tissues with oxygen activates the processes of hematopoiesis. In addition to low hemoglobin, hematocrit, tombocytopenia and leukopenia, a decrease in the total number of red blood cells is noted at this stage. When examining a blood smear, the presence of young forms of erythrocytes is noted: reticulocytes, sometimes erythroblasts.
Similar changes in the blood picture are described in many situational tasks for future doctors.
Symptoms and diagnosis of anemia in chronic bleeding
Chronic posthemorrhagic anemia in its symptoms is similar to iron deficiency, since regular light bleeding leads to a deficiency of this microelement. The course of this blood disease depends on its severity. It is determined depending on the concentration of hemoglobin. Normally, in men it is 135 - 160 g / l, and in women 120 - 140 g / l. In children, this value varies with age from 200 in infants to 150 in adolescents.
Degree of post-hemorrhagic chronic anemia Hemoglobin concentration
- 1 (light) degree 90 – 110 g/l
- 2 degree (moderate) 70 - 90 g/l
- Grade 3 (severe) below 70 g/l
At the initial stage of the development of the disease, patients complain of mild dizziness, flickering "flies" before the eyes, and increased fatigue. Externally noticeable pallor of the skin and mucous membranes.
At the second stage, a decrease in appetite, sometimes nausea, diarrhea, or, conversely, constipation, shortness of breath, is added to the listed symptoms. When listening to heart tones, doctors note heart murmurs characteristic of chronic posthemorrhagic anemia. The condition of the skin also changes: the skin becomes dry, flaky. Painful and inflamed cracks appear in the corners of the mouth. The condition of hair and nails worsens.
Severe anemia is manifested by numbness and tingling in the fingers and toes, specific taste preferences appear, for example, some patients begin to eat chalk, and the perception of smells changes. Very often this stage of chronic posthemorrhagic anemia is accompanied by rapidly progressive caries, stomatitis.
Diagnosis of posthemorrhagic anemia is based on the results of a clinical blood test. In addition to the decrease in the amount of hemoglobin and erythrocytes, characteristic of all types of anemia, a decrease in the color index is detected. Its value ranges from 0.5 - 0.6. In addition, in chronic posthemorrhagic anemia, mutated erythrocytes (microcytes and schizocytes) appear.
Treatment of anemia after massive blood loss
First of all, you need to stop the bleeding. If it is external, then it is necessary to apply a tourniquet, a pressure bandage and take the victim to the hospital. In addition to pallor, cyanosis and clouding of consciousness, severe dryness in the mouth testifies to internal bleeding. At home, it is impossible to help a person in this condition, so stopping internal bleeding is carried out only in a hospital.
After identifying the source and stopping the bleeding, it is urgent to restore the blood supply to the vessels. For this, reopoliglyukin, hemodez, polyglukin are prescribed. Acute blood loss 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 in the introduction of iron preparations and enhanced nutrition to compensate for the deficiency of vitamins and microelements. Ferrum lek, ferlatum, maltofer are usually prescribed.
Usually, the restoration of a normal blood picture occurs after 6 to 8 weeks, but the use of drugs to normalize hematopoiesis continues for up to six months.
Treatment of chronic posthemorrhagic anemia
The first and most important step in the treatment of posthemorrhagic chronic anemia is to determine the source of bleeding and eliminate it. Even the loss of 10-15 ml of blood per day deprives the body of the entire amount of iron that was received with food that day.
A comprehensive examination of the patient is carried out, which necessarily includes consultations with a gastroenterologist, proctologist, hematologist, gynecologist for women, endocrinologist. After identifying the disease that caused the development of chronic posthemorrhagic anemia, its treatment immediately begins.
In parallel, drugs are prescribed that contain iron. For adults, its daily dose is about 100 - 150 mg. Complex agents are prescribed, which, in addition to iron, contain ascorbic acid and B vitamins, which contribute to its better absorption. These are sorbifer durules, ferroplex, fenyuls.
In severe post-hemorrhagic chronic anemia, to stimulate hematopoietic processes, red blood cell transfusion and injection of drugs with iron are indicated. Ferlatum, maltofer, likferr and similar medicines are prescribed.
Recovery after the main course of treatment
The duration of taking iron-containing drugs is determined by the doctor. In addition to the use of various drugs to restore the normal supply of oxygen to the organs and replenish iron stores in the body, good nutrition is very important.
In the diet of a person who has suffered posthemorrhagic anemia, proteins and iron must be present without fail. Preference should be given to meat, eggs, dairy products. The leaders in iron content are organ meats, especially beef liver, meat, fish, caviar, legumes, nuts, buckwheat and oatmeal.
When compiling a diet, attention should be paid not only to how much iron a particular product contains, but also to the degree of its absorption in the body. It increases with the use of vegetables and fruits that contain vitamins B and C. These are citrus fruits, black currants, raspberries, etc.
The course and therapy of posthemorrhagic anemia in children
Posthemorrhagic anemia in children is much more severe, especially its acute form. The clinical picture of this pathology practically does not differ from an adult, but develops faster. And if in an adult a certain amount of lost blood is compensated by the protective reactions of the body, then in a child this can be fatal.
Treatment of acute and chronic forms of posthemorrhagic anemia in children is the same. After identifying the cause and eliminating bleeding, a transfusion of erythrocyte mass is prescribed at the rate of 10-15 ml per kg of weight, iron preparations. Their dosage is calculated individually depending on the severity of anemia and the condition of the child.
For children around six months of age, early introduction of complementary foods is recommended, and should start with foods with a high iron content. Babies are shown the transition to special fortified mixtures. If the disease that led to the development of posthemorrhagic anemia is chronic and cannot be treated, then prophylactic courses of iron preparations must be repeated regularly.
With timely initiation of treatment and non-critical blood loss, the prognosis is generally favorable. After compensation for iron deficiency, the child quickly recovers.
Hypochromic anemia includes several types of anemia in which red blood cells are poorly stained and therefore unable to carry a sufficiently large amount of oxygenated hemoglobin. All types are included in the list of hypochromic anemia, microcytic anemia code 10. Microcytic anemia most often occurs due to the lack of adequate iron stores in the blood. Treatment usually consists of replenishing iron stores.
Microcytic anemia is one of many types of anemia whose characteristic features include an excess of red blood cells. They are small (medically called microcytes), this is normocytic hypochromic anemia. The main measure in the blood count that shows us microcytic anemia is the MCV (Mean Blood Cell Volume). If it is microcytic anemia, the MCV limit is 80 fL (or less).
In the course of microcytic anemia, red blood cells are usually unpigmented (that is, paler). This is due to a deficiency of hemoglobin in the blood cells, measured using the MCHC parameter (mean hemoglobin per erythrocyte).
Hypochromic anemia in children is divided into:
- iron deficiency anemia (the most common cause of anemia in general, considered mild hypochromic anemia);
- thalassemia;
- sideroblastic anemia;
- anemia in chronic diseases (in some cases);
- lead poisoning;
- caused by pyridoxine deficiency.
Hypochromic iron deficiency anemia
Iron deficiency anemia most often occurs due to a lack of adequate iron stores in the blood. This element is necessary for the creation of new red blood cells, its deficiency causes the appearance of diseased red blood cells compared to their healthy counterparts. The disease affects both children and adults.
What is hypochromic anemia and what are its causes? Diagnosis of iron deficiency anemia requires, firstly, determining the cause of the increased demand for this element or a decrease in its reserves in the body. Typical causes of iron deficiency are:
2 blood loss(blood cells contain iron, and the loss of a large volume of blood leads to its deficiency. In women, the most common cause is heavy monthly bleeding; due to stomach ulcers, vascular malformations in the gastrointestinal tract, polyps and colorectal cancer. Sometimes chronic mucositis and blood loss through the digestive tract causes overuse of non-steroidal anti-inflammatory drugs such as Aspirin or Ibuprofen).
3 Improper nutrition(Lack of intake of foods rich in absorbable iron - red meat, eggs, liver, green leafy plants - is often accompanied by the wrong composition of a vegetarian diet).
4 Iron absorption disorders(Many diseases limit the ability of the intestine to absorb iron, such as celiac disease, inflammatory bowel and stomach diseases, and conditions after surgery that removes long sections of the small intestine.)
5 Pregnancy(a state of increased demand for iron - during pregnancy, blood volume increases significantly because the mother's body needs to supply oxygen and nutrients to the developing fetus - a lack of iron can slow down the growth of the fetus).
6 Intravascular hemolysis(under this name, there is excessive destruction of red blood cells in the circulatory system, which can be caused by many factors, such as bacterial toxins).
7 Hemoglobinuria(the abnormal presence of hemoglobin in the urine due to the breakdown of red blood cells, for example, may be accompanied by malaria).
Chronic hypochromic anemia
Diagnosis of microcytic anemia with iron deficiency should be complemented by the exclusion of other equally important causes of this disease.
one . Microcytic anemia can be caused by abnormalities in the structure of hemoglobin chains that occur during a genetic disease called thalassemia. Depending on the type of mutation, the picture of symptoms and the severity of the disease are different. In diagnosis, it is important to accurately collect a medical history to identify similar symptoms in relatives, basic blood tests and detailed molecular diagnostics that identify the mutation that caused the disease.
2 Sideroblastic anemia. This cause of microcytic anemia is poorly understood. It is known to create abnormal cells called sideroblasts. It can be congenital or lifelong (caused by certain medications or other diseases). It is diagnosed by a thorough analysis of the blood picture and the search for factors that cause it to occur.
Symptoms of microcytic anemia
The symptoms of microcytic anemia are very similar to other types of anemia. The most characteristic symptoms of the disease are pallor of the skin (due to a decrease in the content of oxygenated hemoglobin in the tissues), general fatigue, dizziness and weakness. Sometimes, when microcytic anemia continues for many years, the body adjusts to the disease and some symptoms disappear. The disease turns into a severe degree of hypochromic anemia. In severe cases, shortness of breath occurs due to the lack of oxygen in the tissues. Other symptoms of microcytic anemia (which may come or go):
- feeling of fear and feeling threatened;
- irritability;
- chest pain;
- constipation;
- excessive sleepiness;
- mouth ulcers;
- noise in ears;
- cardiopalmus;
- hair loss;
- loss of consciousness or a feeling of impending unconsciousness;
- depression;
- apnea;
- involuntary muscle cramps;
- pale yellow skin;
- nausea;
- burning sensation in the abdomen;
- menstrual disorders (without a cycle);
- inflammation or infection of the surface of the tongue;
- inflammation of the corners of the mouth;
- weakness of appetite;
- difficulty swallowing;
- insomnia;
- restless leg syndrome.
Hypochromic anemia treatment and prognosis
Hypochromic anemia, after establishing the cause, requires causative or symptomatic drug treatment. The most common form, that is, iron deficiency anemia, is treated by supplementing the reserves of this element (for hypochromic anemia, diets and additional drugs prescribed by a doctor are used) and the cause of the disease is eliminated. It is important not only to take medications, but also to eat foods rich in iron. Other conditions that cause hypochromic microcytic anemia require the use of other agents, usually under the supervision of a physician and hematologist.
If the cause of the disease can be identified and eliminated, the prognosis is good. In the case of hypochromic anemia associated, for example, with thalassemia or poisoning, the prognosis depends on the severity of the disease and promptly implemented preventive and therapeutic measures. In some cases, the disease cannot be cured.
Treatment of IDA includes treatment of the pathology that led to iron deficiency, and the use of iron supplements to restore iron stores in the body. Identification and correction of pathological conditions that cause iron deficiency are the most important elements of complex treatment. Routine administration of iron-containing preparations to all patients with IDA is unacceptable, since it is not effective enough, is expensive, and, more importantly, is often accompanied by diagnostic errors (non-detection of neoplasms).
The diet of patients with IDA should include meat products containing iron in the composition of heme, which is absorbed better than from other products. It must be remembered that it is impossible to compensate for a pronounced iron deficiency only by prescribing a diet.
Treatment of iron deficiency is carried out mainly with oral iron-containing preparations, parenteral drugs are used in the presence of special indications. It should be noted that the use of iron-containing oral preparations is effective in most patients whose body is able to adsorb the amount of pharmacological iron sufficient to correct the deficiency. Currently, a large number of preparations containing iron salts are being produced (ferroplex, orferon. Tardiferon). The most convenient and cheapest are preparations containing 200 mg of ferrous sulfate, i.e. 50 mg of elemental iron in one tablet (ferrocal, ferroplex). The usual dose for adults is 1-2 tablets. 3 times a day. Per day, an adult patient should receive at least 3 mg of elemental iron per kg of body weight, i.e., 200 mg per day. The usual dosage for children is 2-3 mg of elemental iron per kg of body weight per day.
The effectiveness of preparations containing ferrous lactate, succinate or fumarate does not exceed the effectiveness of tablets containing ferrous sulfate or gluconate. The combination of iron salts and vitamins in one preparation, with the exception of the combination of iron and folic acid during pregnancy, as a rule, does not increase the absorption of iron. Although this effect can be achieved with high doses of ascorbic acid, the resulting adverse events make the therapeutic use of such a combination impractical. Slow-acting (retard) drugs are usually less effective than regular drugs because they enter the lower intestine where iron is not absorbed, but may be higher than fast-acting drugs taken with food.
It is not recommended to take a break between taking the tablets for less than 6 hours, because within a few hours after taking the drug, duodenal enterocytes are refractory to iron absorption. The maximum absorption of iron occurs when taking tablets on an empty stomach, taking during or after a meal reduces it by 50-60%. Do not take iron supplements with tea or coffee, which inhibit iron absorption.
Most of the adverse events associated with the use of iron-containing preparations are associated with irritation of the gastrointestinal tract. At the same time, adverse events associated with irritation of the lower gastrointestinal tract (moderate constipation, diarrhea) usually do not depend on the dose of the drug, while the severity of irritation of the upper sections (nausea, discomfort, pain in the epigastric region) is determined by the dose. Adverse events are less common in children, although in them the use of iron-containing liquid mixtures can lead to temporary darkening of the teeth. To avoid this, you should give the drug to the root of the tongue, drink the medicine with liquid and brush your teeth more often.
In the presence of severe adverse events associated with irritation of the upper gastrointestinal tract, you can take the drug after meals or reduce the single dose. If adverse events persist, lower iron formulations can be given, such as those in ferrous gluconate (37 mg elemental iron per tablet). If, in this case, adverse effects are not stopped, then you should switch to slow-acting drugs.
Improving the well-being of patients usually begins on the 4th-6th day of adequate therapy, on the 10th-11th day the number of reticulocytes increases, on the 16th-18th day the hemoglobin concentration begins to increase, microcytosis and hypochromia gradually disappear. The average rate of increase in hemoglobin concentration with adequate therapy is 20 g / l for 3 weeks. After 1-1.5 months of successful treatment with iron preparations, their dose can be reduced.
The main reasons for the lack of the expected effect when using iron-containing preparations are presented below. It should be emphasized that the main reason for the ineffectiveness of such treatment is ongoing bleeding, so identifying the source and stopping bleeding is the key to successful therapy.
The main reasons for the ineffectiveness of the treatment of iron deficiency anemia: ongoing blood loss; incorrect drug intake:
- misdiagnosis (anemia in chronic diseases, thalassemia, sideroblastic anemia);
- combined deficiency (iron and vitamin B12 or folic acid);
- taking slow-acting preparations containing iron: malabsorption of iron preparations (rare).
It is important to remember that in order to restore iron stores in the body with a pronounced deficiency, the duration of iron-containing preparations should be at least 4-6 months or at least 3 months after the normalization of hemoglobin in peripheral blood. The use of oral iron preparations does not lead to iron overload, since absorption decreases sharply when iron stores are restored.
Prophylactic use of oral iron preparations is indicated during pregnancy, patients receiving permanent hemodialysis, and blood donors. Premature babies are shown the use of nutritional mixtures containing iron salts.
Patients with IDA rarely require the use of parenteral preparations containing iron (ferrum-lek, imferon, ferkoven, etc.), since they usually respond quickly to treatment with oral preparations. Moreover, adequate oral therapy is usually well tolerated even by patients with gastrointestinal pathology (peptic ulcer, enterocolitis, ulcerative colitis). The main indications for their use are the need for rapid replacement of iron deficiency (significant blood loss, upcoming surgery, etc.), severe side effects of oral medications, or impaired absorption of iron due to damage to the small intestine. Parenteral administration of iron preparations can be accompanied by severe adverse events, as well as lead to excessive accumulation of iron in the body. Parenteral iron preparations do not differ from oral preparations in terms of the rate of normalization of hematological parameters, although the rate of restoration of iron stores in the body with the use of parenteral preparations is much higher. In any case, the use of parenteral iron preparations can only be recommended if the doctor is convinced of the ineffectiveness or intolerance of treatment with oral preparations.
Parenteral iron preparations are usually administered intravenously or intramuscularly, with the intravenous route of administration being preferred. They contain 20 to 50 mg of elemental iron per ml. The total dose of the drug is calculated by the formula:
Dose of iron (mg) = (Hemoglobin deficiency (g / l)) / 1000 (Volume of circulating blood) x 3.4.
The volume of circulating blood in adults is approximately 7% of body weight. To restore iron stores, 500 mg is usually added to the calculated dose. Before starting therapy, 0.5 ml of the drug is administered to exclude an anaphylactic reaction. If within 1 hour there are no signs of anaphylaxis, then the drug is administered so that the total dose is 100 mg. After that, 100 mg is administered daily until the total dose of the drug is reached. All injections are given slowly (1 ml per minute).
An alternative method is the simultaneous intravenous administration of the entire total dose of iron. The drug is dissolved in 0.9% sodium chloride solution so that its concentration is less than 5%. The infusion is started at a rate of 10 drops per minute, in the absence of adverse events within 10 minutes, the rate of administration is increased so that the total duration of the infusion is 4-6 hours.
The most severe side effect of parenteral iron preparations is an anaphylactic reaction, which can occur with both intravenous and intramuscular administration. Although such reactions are relatively rare, the use of parenteral iron preparations should be carried out only in hospitals equipped to provide full emergency care. Other adverse events include flushing of the face, fever, urticaria, arthralgia and myalgia, phlebitis (with too rapid administration of the drug). Drugs should not get under the skin. The use of parenteral iron preparations can lead to the activation of rheumatoid arthritis.
Red blood cell transfusions are carried out only in case of severe IDA, accompanied by severe signs of circulatory failure, or the upcoming surgical treatment.