Conductible ICD anemia. Symptoms and treatment of anemia Chronic postgemorrhagic anemia Code of ICD 10
The ICD-10 has been introduced into the practice of health throughout the territory of the Russian Federation in 1999 by order of the Ministry of Health of Russia from 27.05.97. №170
A new revision (ICD-11) is planned to be planned in 2017 2018.
With changes and additions to WHO.
Processing and transferring changes © MKB-10.com
ICD 10. Class III (D50-D89)
ICD 10. Class III. Blood diseases, hematopoietic organs and separate disorders involving the immune mechanism (D50-D89)
Excelves: autoimmune disease (system) BDU (M35.9), individual states arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and postpartum period (O00-O99), congenital anomalies, deformations and chromosomal disorders (Q00- Q99), endocrine diseases, nutrition disorders and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), injury, poisoning and some other effects of exposure external reasons (S00-T98), neoplasms (C00-D48), symptoms, signs and deviations from the norm identified during clinical and laboratory studies, not classified in other categories (R00-R99)
This class contains the following blocks:
D50-D53 Feedback Anemia
D55-D59 hemolytic anemia
D60-D64 aplastic and other anemia
D65-D69 Blood coagulation disorders, purpura and other hemorrhagic states
D70-D77 Other diseases of blood and hematopoietic organs
D80-D89 separate disorders involving the immune mechanism
An asterisk marked the following categories:
D77 Other blood disorders and blood-forming organs in diseases classified in other categories
Feedback anemia (D50-D53)
D50 Conductible anemia
D50.0 Conductive anemia Secondary due to blood loss (chronic). Postgymorrhagic (chronic) anemia.
Excelves: acute postgemorrhagic anemia (D62) innate anemia due to blood loss in the fetus (P61.3)
D50.1 Siderophenic dysfagia. Kelly Paterson Syndrome. Plammere-Visson syndrome
D50.8 Other iron deficiency anemia
D50.9 Conductable Anemia Uncomfortable
D51 Vitamin-B12 deficient anemia
Excluded: Vitamin B12 deficiency (E53.8)
D51.0 Vitamin-B12 deficient anemia due to the deficit of the internal factor.
Congenital insufficiency of the internal factor
D51.1 Vitamin-B12 deficient anemia due to selective violation of the absorption of vitamin B12 with proteinuria.
Immerslund syndrome (-Gresbek). Megaloblastic hereditary anemia
D51.2 TransCoublemin II shortage
D51.3 Other vitamin-B12-deficient powers related to nutrition. Vegetarian anemia
D51.8 Other Vitamin B12 deficient anemia
D51.9 Vitamin-B12 deficient anemia unspecified
D52 Foliowfoot anemia
D52.0 Foliofertification of nutritional anemia. Megaloblastic alimentary anemia
D52.1 Folieviced medication anemia. If necessary, identify the drug
use additional external reasons (class XX)
D52.8 Other Foliudiform Anemia
D52.9 Foliow defective anemia is unspecified. Anemia due to insufficient entry into the body folic acid, BDA
D53 Other food-related anemia
Included: Megaloblastic anemia, which cannot be treated
mr. B12 or Folate
D53.0 anemia due to protein failure. Anemia due to the insufficiency of amino acids.
Excluded: Lesha-Nihena syndrome (E79.1)
D53.1 Other megaloblastic anemia, not classified in other categories. Megaloblastic anemia BDU.
Excluded: Disea Gulielmo disease (C94.0)
D53.2 Anemia caused by Qing.
Excluded: qing (E54)
D53.8 Other refined powered anemia.
Anemia associated with a deficit:
Excluded: deficiency failure without mentioning
anemia, such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Anemia associated with food, unspecified. Simple chronic anemia.
Excluded: Anemia BDU (D64.9)
Hemolytic anemia (D55-D59)
D55 anemia due to enzyme violations
Excended: enzymestic anemia caused by drugs (D59.2)
D55.0 Anemia due to the insufficiency of glucose-6-phosphate dehydrogenase [G-6-FD]. Faviism. Mr. FD-deficient anemia
D55.1 Anemia due to other violations of glutathionic metabolism.
Anemia due to lack of enzymes (with the exception of Mr. FD) associated with hexosomonophosphate [GMF]
metabolic path shunt. Hemolytic nonferrabic anemia (hereditary) type 1
D55.2 Anemia due to violations of glycolytic enzymes.
Gemolytic nonferrabic (hereditary) type II
Due to the insufficiency of hexokinase
Due to the insufficiency of Piruvatakinase
Due to the lack of trioseophosphatisomerase
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme violations
D55.9 Anemia due to the uncomfortable enzyme violation
D56 Thalassemia
Excluded: waterfront fetal due to hemolytic disease (P56. -)
D56.1 beta-thalassemia. Anemia Kuli. Heavy beta-thalassemia. Sick-shaped cell beta-thalassemia.
D56.3 Wear a sign of thalassemia
D56.4 hereditary persistence of fetal hemoglobin [NPFG]
D56.9 Thalassemia unspecified. Mediterranean anemia (with another hemoglobinopathy)
Thalassemia (small) (mixed) (with another hemoglobinopathy)
D57 Sickle-cellular violations
Excluded: other hemoglobinopathy (D58. -)
sick-shaped cell beta-thalassemia (D56.1)
D57.0 Sickle-cell anemia with crisis. HB-SS disease with crisis
D57.1 Sickle-cell anemia without chisosis.
D57.2 Double heterozygous sickle cellular disorders
D57.3 Signal of Self-Cellity Signs. Hemoglobin S.Geredozygous Hemoglobin S
D57.8 Other Sickle Cellular Disorders
D58 Other hereditary hemolytic anemia
D58.0 hereditary spherocytosis. Akholuric (family) jaundice.
Congenital (spherocitur) hemolytic jaundice. Minkowski-Shoffar Syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalcithosis (congenital) (hereditary)
D58.2 Other hemoglobinopathy. Abnormal hemoglobin BDU. Congenital anemia with Heinz Tales.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy BDU.
Excluded: Family Policytemy (D75.0)
hB-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
polycithimera associated with a height (D75.1)
D58.8 Other refined hereditary hemolytic anemia. Stomatocytosis
D58.9 hereditary hemolytic anemia Unclean
D59 Acquired hemolytic anemia
D59.0 Medical autoimmune hemolytic anemia.
If necessary, identify the drug use an additional external reasons (class XX).
D59.1 Other autoimmune hemolytic anemia. An autoimmune hemolytic disease (cold type) (thermal type). Chronic disease caused by cold hemagglutinins.
Cold Type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excelves: Evans Syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Medical Nautualimmune hemolytic anemia. Medical fermented anemia.
If necessary, identify the drug use additional external reasons (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other nonautimmune hemolytic anemia.
If necessary, identify the cause uses an additional external cause code (class XX).
D59.5 Paroxysmal Night Hemoglobinuria [Markiafa-Mikeli].
D59.6 Hemoglobinuria due to hemolysis caused by other external reasons.
Excended: Hemoglobinuria BDU (R82.3)
D59.8 Other acquired hemolytic anemia
D59.9 Acquired hemolytic anemia is unspecified. Idiopathic hemolytic anemia chronic
Aplastic and other anemia (D60-D64)
D60 Acquired Net Flushing Aplasia (Erythroblasting)
Included: Red-cell aplasia (purchased) (adults) (with a timome)
D60.0 Chronic Acquired Pure Red Shell Aplasia
D60.1 Transient Acquired Pure Flushing Aplasia
D60.8 Other purchased clean color Aplasia
D60.9 Acquired Clean Flushing Aplasia Uncomfortable
D61 Other aplastic anemia
Excluded: Agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) color-cell:
Flemfena-Daemond Syndrome. Family hypoplastic anemia. Anemia Fanconi. Panciton with defects
D61.1 Medical aplastic anemia. If necessary, identify the drug
use additional external reasons (class XX).
D61.2 Aplastic anemia caused by other external agents.
If necessary, identify the cause uses an additional external cause code (class XX).
D61.3 idiopathic aplastic anemia
D61.8 Other refined aplastic anemia
D61.9 Aplastic anemia is unspecified. Hypoplastic anemia BDA. Gapopia bone marrow. Pämaleftiz
D62 Acute PostGemorrhagic Anemia
Excluded: Congenital anemia due to blood loss in the fetus (P61.3)
D63 anemia in chronic diseases classified in other categories
D63.0 Anemia with neoplasms (C00-D48 +)
D63.8 Anemia with other chronic diseases classified in other categories
D64 Other anemia
Excelves: Refractory anemia:
With an excess of blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
Without sideroblasts (D46.0)
D64.0 Hereditary Cideroblastic anemia. Floor-related hypochromic stud loan anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, identify the disease use additional code.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If necessary, identify the cause uses an additional external cause code (class XX).
D64.3 Other sederoblastic anemia.
Pyridoxinreaging, not classified in other categories
D64.4 Congenital DysierTropoietic anemia. Dzhemopoietic anemia (congenital).
Excluded: Blackfen Daemond Syndrome (D61.0)
disea Gulielmo disease (C94.0)
D64.8 Other updated anemia. Children's pseudoleikosis. Leukoeritroblastic anemia
Blood coagulation disorders, purpura and others
Hemorrhagic States (D65-D69)
D65 Disseminated intravascular coagulation [Defibrification syndrome]
Afibrinogenemia purchased. Coagulopathy consumption
Diffuse or disseminated intravascular coagulation
Fibrinolytic bleeding acquired
Excluded: Defibrination syndrome (complicating):
In the newborn (P60)
D66 hereditary deficit of factor VIII
Factor deficiency VIII (with a functional impairment)
Excluded: Factor deficiency VIII with vascular violation (D68.0)
D67 hereditary deficit of IX factor
Factor IX (with a functional impairment)
The thromboplastic component of plasma
D68 Other Breasurance Disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and postpartum period (O45.0, O46.0, O67.0, O72.3)
D68.0 Willebrand disease. Angichemophilia. Factor deficiency VIII with vascular violation. Vascular hemophilia.
Excluded: Sapacity of capillaries hereditary (D69.8)
factor deficiency VIII:
With functional impairment (D66)
D68.1 Inheritant deficiency of Factor XI. Hemophilia S. Plasma Thromboplast Predecessor
D68.2 Inheritance deficit of other coagulation factors. Congenital Afibrinogenemia.
Dysfibrinegenemia (congenital). Vgipoconverteria. Ovrine's disease
D68.3 Hemorrhagic disorders caused by anticoagulant circulating blood. Hypergelinemia.
If necessary, identify the used anticoagulant uses an additional external cause code.
D68.4 Acquired shortage of coagulation factor.
Cutting factor deficiency due to:
Vitamin K. Insufficiency
Excluded: Vitamin K insufficiency in a newborn (P53)
D68.8 Other refined collaboration disorders. Presence of the system of system red lupus inhibitor
D68.9 Unspecified coagulation violation
D69 Purpur and other hemorrhagic states
Excluded: Benign Hypergammaglobulinemic Purple (D89.0)
cryoglobululmic Purple (D89.1)
idiopathic (hemorrhagic) thrombocytemia (D47.3)
lightning Purple (D65)
thrombotic thrombocytopenic purple (M31.1)
D69.0 Allergic Purple.
D69.1 Quality platelet defects. Bernard Sulieus syndrome [hygounts platelets].
Glanzmann's disease. Sound platelet syndrome. Thrombaste (hemorrhagic) (hereditary). Thrombocytopathy.
Excended: Willebrand Disease (D68.0)
D69.2 Other low-profacitone purple.
D69.3 Idiopathic thrombocytopenic purple. Evans syndrome
D69.4 Other primary thrombocytopenia.
Excluded: thrombocytopenia with the absence of radiation bone (Q87.2)
transient neonatal thrombocytopenia (P61.0)
syndrome Viscott-Aldrich (D82.0)
D69.5 Secondary thrombocytopenia. If necessary, identify the cause uses an additional external cause code (class XX).
D69.6 Thrombocytopenia uncomfortable
D69.8 Other refined hemorrhagic states. Sapacity of capillaries (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic State of Uncomfortable
Other diseases of blood and hematopoietic organs (D70-D77)
D70 Agranulocytosis
Agranulocyte angina. Children's genetic agranulocytosis. Kostmanna disease
If necessary, identify the drug that caused neutropenia use an additional external cause code (class XX).
Excluded: Transient Neonatal Neutropenia (P61.5)
D71 Functional disorders of polymorphic nuclear neutrophils
Defect of the receptor complex of the cell membrane. Chronic (children) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other Disorders of White Blood Cells
Excelves: Basophilia (D75.8)
immune disorders (D80-D89)
preycloth (syndrome) (D46.9)
D72.0 Genetic leukocyte anomalies.
Anomaly (granulation) (granulocyte) or syndrome:
Excluded: Chadiak Higashi (-Stainbrick) syndrome (E70.3)
D72.8 Other refined disorders of white blood cells.
Leukocytosis. Lymphocytosis (symptomatic). Lymphonia. Monocytosis (symptomatic). Plasmacytosis
D72.9 Uncomfortable White Blood Cell Violation
D73 Diseases of the spleen
D73.0 hypipens. After postoperative. Atrophy of the spleen.
Excluded: Aspins (congenital) (Q89.0)
D73.2 chronic stagnant splenomegaly
D73.5 Infarct spleen. Spiece break Non-immote. Recretting the spleen.
Excluded: traumatic spleen break (S36.0)
D73.8 Other diseases of the spleen. Fibrosis spleen BDU. Perisplanite. Splenit BDA
D73.9 Uncomfortable spleen disease
D74 methemoglobiney
D74.0 congenital methemoglobinemia. Congenital deficiency of Nadh-methemoglobinreductase.
Hemoglobinosis m [HB-M disease] .methemoglobinemia hereditary
D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfgemoglobinemia).
Toxic methemoglobinemia. If necessary, identify the cause uses an additional external cause code (class XX).
D74.9 Unspecified methemoglobinemia
D75 Other blood diseases and hematopoietic organs
Excluded: Increase lymph nodes (R59. -)
hypergammaglobulinemia BDU (D89.2)
Mesenter (acute) (chronic) (i88.0)
Excluded: hereditary ovalcitosis (D58.1)
D75.1 Secondary polycythemia.
Reducing plasma volume
D75.2 Essential thrombocytosis.
Excended: Essential (hemorrhagic) thrombocytemy (D47.3)
D75.8 Other refined blood diseases and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs unspecified
D76 Separate diseases leaking with the involvement of lymphorticular tissue and reticulogistic system
Excelves: Letter Eleer-Sive (C96.0)
malignant histiocytosis (C96.1)
reticulosendotelia or reticulosis:
GiStiocyte medullar (C96.1)
D76.0 histiocytosis from Langerhans cells, not classified in other categories. Eosinophilic granuloma.
Disease Handa-Shuller-Chisgen. Histiocytosis x (chronic)
D76.1 Hemophagocytic lymphogistiocytosis. Family hemophagocytic reticulosis.
Gisticiocytosis from mononuclear phagocytes other than Langerhans cells, BDU
D76.2 Hemophagocytic syndrome associated with infection.
If necessary, identify the infectious pathogen or the disease use the additional code.
D76.3 Other histiocytosis syndromes. Reticulogisticiocytoma (giant).
Sine histiocytosis with massive lymphadenopathy. Xantograntulm
D77 Other blood disorders and hematopoietic organs in diseases classified in other categories.
Fibrosis of the spleen with schistosomes [Bilgarciosis] (B65. -)
Separate disorders involving the immune mechanism (D80-D89)
Included: defects in the complement system, immunodeficiency disorders, with the exception of the disease,
caused by a human immunodeficiency virus [HIV] sarcoidosis
Excelves: autoimmune diseases (system) BDU (M35.9)
functional disorders of polymorphic nuclear neutrophils (D71)
disease caused by human immunodeficiency virus [HIV] (B20-B24)
D80 immunodeficiency with predominant antibody failure
D80.0 hereditary hypogammaglobulinemia.
Autosomal recessive Aghamaglobulinemia (Swiss type).
Captured with X-chromosome Aghamaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Unseasonal hypogammaglobulinemia. Agamaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General Aghamaglobulinemia. Hypogammaglobulinemia BDA
D80.2. Election deficit Immunoglobulin A.
D80.3 Selective deficit of immunoglobulin g
D80.4 Election deficit Immunoglobulin M
D80.5 Immunodifying Immunoglobulin M
D80.6 Insufficiency of antibodies with close to normal level of immunoglobulins or with hyperimmunoglobulinemia.
Deficiency of antibodies with hyperimmunoglobulinemia
D80.7 Transient Highogamaglobulinemia Children
D80.8 Other immunodeficiency with the predominant defect of antibodies. Capppa-light chain deficiency
D80.9 Immunodeficiency with the predominant defect of antibody unspecified
D81 Combined immunodeficiency
Excluded: Autosomal Recessive Agamaglobulinemia (Swiss Type) (D80.0)
D81.0 Heavy Combined Immunodeficiency with Retic Dysgenesis
D81.1 Heavy Combined Immunodeficiency with Low T- and B-Cells
D81.2 Heavy Combined Immunodeficiency with Low or normal content B-cells
D81.3 Deficity of adenosine formation
D81.5 The deficiency of purrunucleosidephosphorylase
D81.6 Laptop of class I molecules of the main histocompatibility complex. Syndrome "Nude lymphocytes"
D81.7 Laptop Molecules of Class II main histocompatibility complex
D81.8 Other combined immunodeficiency. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency is unspecified. Heavy Combined Imundage Upholstery BDU
D82 Immunodeficiency associated with other significant defects
Excluded: Atthantic Teleangectasia [Louis Bar] (G11.3)
D82.0 Wiscott-Oldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di George syndrome. Syndrome diverticula pharynges.
Aplasia or hypoplasia with immune failure
D82.2 Immunodeficiency with dwarfship due to short limbs
D82.3 Immunodeficiency due to hereditary defect caused by the Epstein-Barr virus.
Captured with X-chromosome lymphoproliferative disease
D82.4 Hyperimmunoglobulin E Syndrome
D82.8 Immunodeficiency associated with other refined significant defects
D82.9 Immunodeficiency associated with a significant defect, unspecified
D83 Normal Variable Immunodeficiency
D83.0 Common variable immunodeficiency with predominant deviations in the amount and functional activity of B-cells
D83.1 Common Variable Immunodeficiency with the predominance of impairment of immunoregulatory T-cells
D83.2 Common Variable Immunodeficiency with Autoantales to B- or T-Cells
D83.8 Other common variable immunodeficiency
D83.9 Common Variable Immunodeficiency Unclean
D84 Other Immunodeficiencies
D84.0 Defect functional antigen-1 lymphocytes
D84.1 Defect in the complement system. Esterase Inhibitor C1 deficiency
D84.8 Other updated immunodeficiency violations
D84.9 Immunodeficiency is uncomfortable
D86 sarcoidosis
D86.1 Sarcoidosis of lymphatic nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of lymph nodes
D86.8 Sarcoidosis of other updated and combined localizations. Iridocyclic with sarcoidosis (H22.1).
Multiple paralysis of clerk nerves during sarcoidosis (G53.2)
Investigating fever [Herford's disease]
D86.9 Sarcoidosis uncomfortable
D89 Other disorders with the involvement of the immune mechanism, not classified in other categories
Excluded: Hyperglobulinemia BDU (R77.1)
monoclonal gammapaty (D47.2)
sustice and transplant rejection (T86 -)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purple. Polyclonal gammapathy BDA
D89.2 hypergammaglobulinemia uncomfortable
D89.8 Other refined violations with the involvement of the immune mechanism not classified in other categories
D89.9 Violation involving the immune mechanism is unspecified. Immune disease BDA
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Code of ICD: D50
Iron-deficiency anemia
Iron-deficiency anemia
Code of the ICD Online / Code of the ICD D50 / International Classification of Diseases / Diseases of Blood, Hydraulic Organs and Separate Disorders involving the immune mechanism / anemia related to nutrition / iron deficiency anemia
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ICD 10. Class III. Blood diseases, hematopoietic organs and separate disorders involving the immune mechanism (D50-D89)
Excelves: autoimmune disease (system) BDU (M35.9), individual states arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and postpartum period (O00-O99), congenital anomalies, deformations and chromosomal disorders (Q00- Q99), endocrine diseases, nutrition disorders and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), injuries, poisoning and some other effects of external reasons (S00-T98), neoplasms (C00-D48), symptoms, signs and deviations from the norm identified during clinical and laboratory studies, not classified in other categories (R00-R99)
This class contains the following blocks:
D50-D53 Feedback Anemia
D55-D59 hemolytic anemia
D60-D64 aplastic and other anemia
D65-D69 Blood coagulation disorders, purpura and other hemorrhagic states
D70-D77 Other diseases of blood and hematopoietic organs
D80-D89 separate disorders involving the immune mechanism
An asterisk marked the following categories:
D77 Other blood disorders and blood-forming organs in diseases classified in other categories
Feedback anemia (D50-D53)
D50 Conductible anemia
D50.0 Conductive anemia Secondary due to blood loss (chronic). Postgymorrhagic (chronic) anemia.
Excelves: acute postgemorrhagic anemia (D62) innate anemia due to blood loss in the fetus (P61.3)
D50.1 Siderophenic dysfagia. Kelly Paterson Syndrome. Plammere-Visson syndrome
D50.8 Other iron deficiency anemia
D50.9 Conductable Anemia Uncomfortable
D51 Vitamin-B12 deficient anemia
Excluded: Vitamin B12 deficiency (E53.8)
D51.0 Vitamin-B12 deficient anemia due to the deficit of the internal factor.
Congenital insufficiency of the internal factor
D51.1 Vitamin-B12 deficient anemia due to selective violation of the absorption of vitamin B12 with proteinuria.
Immerslund syndrome (-Gresbek). Megaloblastic hereditary anemia
D51.2 TransCoublemin II shortage
D51.3 Other vitamin-B12-deficient powers related to nutrition. Vegetarian anemia
D51.8 Other Vitamin B12 deficient anemia
D51.9 Vitamin-B12 deficient anemia unspecified
D52 Foliowfoot anemia
D52.0 Foliofertification of nutritional anemia. Megaloblastic alimentary anemia
D52.1 Folieviced medication anemia. If necessary, identify the drug
use additional external reasons (class XX)
D52.8 Other Foliudiform Anemia
D52.9 Foliow defective anemia is unspecified. Anemia caused by insufficient admission to folic acid organism, BD
D53 Other food-related anemia
Included: Megaloblastic anemia, which cannot be treated
mr. B12 or Folate
D53.0 anemia due to protein failure. Anemia due to the insufficiency of amino acids.
Excluded: Lesha-Nihena syndrome (E79.1)
D53.1 Other megaloblastic anemia, not classified in other categories. Megaloblastic anemia BDU.
Excluded: Disea Gulielmo disease (C94.0)
D53.2 Anemia caused by Qing.
Excluded: qing (E54)
D53.8 Other refined powered anemia.
Anemia associated with a deficit:
Excluded: deficiency failure without mentioning
anemia, such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Anemia associated with food, unspecified. Simple chronic anemia.
Excluded: Anemia BDU (D64.9)
Hemolytic anemia (D55-D59)
D55 anemia due to enzyme violations
Excended: enzymestic anemia caused by drugs (D59.2)
D55.0 Anemia due to the insufficiency of glucose-6-phosphate dehydrogenase [G-6-FD]. Faviism. Mr. FD-deficient anemia
D55.1 Anemia due to other violations of glutathionic metabolism.
Anemia due to lack of enzymes (with the exception of Mr. FD) associated with hexosomonophosphate [GMF]
metabolic path shunt. Hemolytic nonferrabic anemia (hereditary) type 1
D55.2 Anemia due to violations of glycolytic enzymes.
Gemolytic nonferrabic (hereditary) type II
Due to the insufficiency of hexokinase
Due to the insufficiency of Piruvatakinase
Due to the lack of trioseophosphatisomerase
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme violations
D55.9 Anemia due to the uncomfortable enzyme violation
D56 Thalassemia
Excluded: waterfront fetal due to hemolytic disease (P56. -)
D56.1 beta-thalassemia. Anemia Kuli. Heavy beta-thalassemia. Sick-shaped cell beta-thalassemia.
D56.3 Wear a sign of thalassemia
D56.4 hereditary persistence of fetal hemoglobin [NPFG]
D56.9 Thalassemia unspecified. Mediterranean anemia (with another hemoglobinopathy)
Thalassemia (small) (mixed) (with another hemoglobinopathy)
D57 Sickle-cellular violations
Excluded: other hemoglobinopathy (D58. -)
sick-shaped cell beta-thalassemia (D56.1)
D57.0 Sickle-cell anemia with crisis. HB-SS disease with crisis
D57.1 Sickle-cell anemia without chisosis.
D57.2 Double heterozygous sickle cellular disorders
D57.3 Signal of Self-Cellity Signs. Hemoglobin S.Geredozygous Hemoglobin S
D57.8 Other Sickle Cellular Disorders
D58 Other hereditary hemolytic anemia
D58.0 hereditary spherocytosis. Akholuric (family) jaundice.
Congenital (spherocitur) hemolytic jaundice. Minkowski-Shoffar Syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalcithosis (congenital) (hereditary)
D58.2 Other hemoglobinopathy. Abnormal hemoglobin BDU. Congenital anemia with Heinz Tales.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy BDU.
Excluded: Family Policytemy (D75.0)
hB-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
polycithimera associated with a height (D75.1)
D58.8 Other refined hereditary hemolytic anemia. Stomatocytosis
D58.9 Hereditary hemolytic anemia unspecified
D59 Acquired hemolytic anemia
D59.0 Medical autoimmune hemolytic anemia.
If necessary, identify the drug use an additional external reasons (class XX).
D59.1 Other autoimmune hemolytic anemia. An autoimmune hemolytic disease (cold type) (thermal type). Chronic disease caused by cold hemagglutinins.
Cold Type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excelves: Evans Syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Medical Nautualimmune hemolytic anemia. Medical fermented anemia.
If necessary, identify the drug use additional external reasons (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other nonautimmune hemolytic anemia.
If necessary, identify the cause uses an additional external cause code (class XX).
D59.5 Paroxysmal Night Hemoglobinuria [Markiafa-Mikeli].
D59.6 Hemoglobinuria due to hemolysis caused by other external reasons.
Excended: Hemoglobinuria BDU (R82.3)
D59.8 Other acquired hemolytic anemia
D59.9 Acquired hemolytic anemia is unspecified. Idiopathic hemolytic anemia chronic
D60 Acquired Net Flushing Aplasia (Erythroblasting)
Included: Red-cell aplasia (purchased) (adults) (with a timome)
D60.0 Chronic Acquired Pure Red Shell Aplasia
D60.1 Transient Acquired Pure Flushing Aplasia
D60.8 Other purchased clean color Aplasia
D60.9 Acquired Clean Flushing Aplasia Uncomfortable
D61 Other aplastic anemia
Excluded: Agranulocytosis (D70)
D61.0 Constitutional aplastic anemia.
Aplasia (pure) color-cell:
Flemfena-Daemond Syndrome. Family hypoplastic anemia. Anemia Fanconi. Panciton with defects
D61.1 Medical aplastic anemia. If necessary, identify the drug
use additional external reasons (class XX).
D61.2 Aplastic anemia caused by other external agents.
If necessary, identify the cause uses an additional external cause code (class XX).
D61.3 idiopathic aplastic anemia
D61.8 Other refined aplastic anemia
D61.9 Aplastic anemia is unspecified. Hypoplastic anemia BDA. Bone marrow hypoplasia. Pämaleftiz
D62 Acute PostGemorrhagic Anemia
Excluded: Congenital anemia due to blood loss in the fetus (P61.3)
D63 anemia in chronic diseases classified in other categories
D63.0 Anemia with neoplasms (C00-D48 +)
D63.8 Anemia with other chronic diseases classified in other categories
D64 Other anemia
With an excess of blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
Without sideroblasts (D46.0)
D64.0 Hereditary Cideroblastic anemia. Floor-related hypochromic stud loan anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, identify the disease use additional code.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If necessary, identify the cause uses an additional external cause code (class XX).
D64.3 Other sederoblastic anemia.
Pyridoxinreaging, not classified in other categories
D64.4 Congenital DysierTropoietic anemia. Dzhemopoietic anemia (congenital).
Excluded: Blackfen Daemond Syndrome (D61.0)
disea Gulielmo disease (C94.0)
D64.8 Other updated anemia. Children's pseudoleikosis. Leukoeritroblastic anemia
Blood coagulation disorders, purpura and others
Hemorrhagic States (D65-D69)
D65 Disseminated intravascular coagulation [Defibrification syndrome]
Afibrinogenemia purchased. Coagulopathy consumption
Diffuse or disseminated intravascular coagulation
Fibrinolytic bleeding acquired
Excluded: Defibrination syndrome (complicating):
In the newborn (P60)
D66 hereditary deficit of factor VIII
Factor deficiency VIII (with a functional impairment)
Excluded: Factor deficiency VIII with vascular violation (D68.0)
D67 hereditary deficit of IX factor
Factor IX (with a functional impairment)
The thromboplastic component of plasma
D68 Other Breasurance Disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and postpartum period (O45.0, O46.0, O67.0, O72.3)
D68.0 Willebrand disease. Angichemophilia. Factor deficiency VIII with vascular violation. Vascular hemophilia.
Excluded: Sapacity of capillaries hereditary (D69.8)
factor deficiency VIII:
With functional impairment (D66)
D68.1 Inheritant deficiency of Factor XI. Hemophilia S. Plasma Thromboplast Predecessor
D68.2 Inheritance deficit of other coagulation factors. Congenital Afibrinogenemia.
Dysfibrinegenemia (congenital). Vgipoconverteria. Ovrine's disease
D68.3 Hemorrhagic disorders caused by anticoagulant circulating blood. Hypergelinemia.
If necessary, identify the used anticoagulant uses an additional external cause code.
D68.4 Acquired shortage of coagulation factor.
Cutting factor deficiency due to:
Vitamin K. Insufficiency
Excluded: Vitamin K insufficiency in a newborn (P53)
D68.8 Other refined collaboration disorders. Presence of the system of system red lupus inhibitor
D68.9 Unspecified coagulation violation
D69 Purpur and other hemorrhagic states
Excluded: Benign Hypergammaglobulinemic Purple (D89.0)
cryoglobululmic Purple (D89.1)
idiopathic (hemorrhagic) thrombocytemia (D47.3)
lightning Purple (D65)
thrombotic thrombocytopenic purple (M31.1)
D69.0 Allergic Purple.
D69.1 Quality platelet defects. Bernard Sulieus syndrome [hygounts platelets].
Glanzmann's disease. Sound platelet syndrome. Thrombaste (hemorrhagic) (hereditary). Thrombocytopathy.
Excended: Willebrand Disease (D68.0)
D69.2 Other low-profacitone purple.
D69.3 Idiopathic thrombocytopenic purple. Evans syndrome
D69.4 Other primary thrombocytopenia.
Excluded: thrombocytopenia with the absence of radiation bone (Q87.2)
transient neonatal thrombocytopenia (P61.0)
syndrome Viscott-Aldrich (D82.0)
D69.5 Secondary thrombocytopenia. If necessary, identify the cause uses an additional external cause code (class XX).
D69.6 Thrombocytopenia uncomfortable
D69.8 Other refined hemorrhagic states. Sapacity of capillaries (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic State of Uncomfortable
Other diseases of blood and hematopoietic organs (D70-D77)
D70 Agranulocytosis
Agranulocyte angina. Children's genetic agranulocytosis. Kostmanna disease
If necessary, identify the drug that caused neutropenia use an additional external cause code (class XX).
Excluded: Transient Neonatal Neutropenia (P61.5)
D71 Functional disorders of polymorphic nuclear neutrophils
Defect of the receptor complex of the cell membrane. Chronic (children) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other Disorders of White Blood Cells
Excelves: Basophilia (D75.8)
immune disorders (D80-D89)
preycloth (syndrome) (D46.9)
D72.0 Genetic leukocyte anomalies.
Anomaly (granulation) (granulocyte) or syndrome:
Excluded: Chadiak Higashi (-Stainbrick) syndrome (E70.3)
D72.8 Other refined disorders of white blood cells.
Leukocytosis. Lymphocytosis (symptomatic). Lymphonia. Monocytosis (symptomatic). Plasmacytosis
D72.9 Uncomfortable White Blood Cell Violation
D73 Diseases of the spleen
D73.0 hypipens. After postoperative. Atrophy of the spleen.
Excluded: Aspins (congenital) (Q89.0)
D73.2 chronic stagnant splenomegaly
D73.5 Infarct spleen. Spiece break Non-immote. Recretting the spleen.
Excluded: traumatic spleen break (S36.0)
D73.8 Other diseases of the spleen. Fibrosis spleen BDU. Perisplanite. Splenit BDA
D73.9 Uncomfortable spleen disease
D74 methemoglobiney
D74.0 congenital methemoglobinemia. Congenital deficiency of Nadh-methemoglobinreductase.
Hemoglobinosis m [HB-M disease] .methemoglobinemia hereditary
D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfgemoglobinemia).
Toxic methemoglobinemia. If necessary, identify the cause uses an additional external cause code (class XX).
D74.9 Unspecified methemoglobinemia
D75 Other blood diseases and hematopoietic organs
Excelves: an increase in lymph nodes (R59. -)
hypergammaglobulinemia BDU (D89.2)
Mesenter (acute) (chronic) (i88.0)
Excluded: hereditary ovalcitosis (D58.1)
D75.1 Secondary polycythemia.
Reducing plasma volume
D75.2 Essential thrombocytosis.
Excended: Essential (hemorrhagic) thrombocytemy (D47.3)
D75.8 Other refined blood diseases and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs unspecified
D76 Separate diseases leaking with the involvement of lymphorticular tissue and reticulogistic system
Excelves: Letter Eleer-Sive (C96.0)
malignant histiocytosis (C96.1)
reticulosendotelia or reticulosis:
GiStiocyte medullar (C96.1)
D76.0 histiocytosis from Langerhans cells, not classified in other categories. Eosinophilic granuloma.
Disease Handa-Shuller-Chisgen. Histiocytosis x (chronic)
D76.1 Hemophagocytic lymphogistiocytosis. Family hemophagocytic reticulosis.
Gisticiocytosis from mononuclear phagocytes other than Langerhans cells, BDU
D76.2 Hemophagocytic syndrome associated with infection.
If necessary, identify the infectious pathogen or the disease use the additional code.
D76.3 Other histiocytosis syndromes. Reticulogisticiocytoma (giant).
Sine histiocytosis with massive lymphadenopathy. Xantograntulm
D77 Other blood disorders and hematopoietic organs in diseases classified in other categories.
Fibrosis of the spleen with schistosomes [Bilgarciosis] (B65. -)
Separate disorders involving the immune mechanism (D80-D89)
Included: defects in the complement system, immunodeficiency disorders, with the exception of the disease,
caused by a human immunodeficiency virus [HIV] sarcoidosis
Excelves: autoimmune diseases (system) BDU (M35.9)
functional disorders of polymorphic nuclear neutrophils (D71)
disease caused by human immunodeficiency virus [HIV] (B20-B24)
D80 immunodeficiency with predominant antibody failure
D80.0 hereditary hypogammaglobulinemia.
Autosomal recessive Aghamaglobulinemia (Swiss type).
Captured with X-chromosome Aghamaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Unseasonal hypogammaglobulinemia. Agamaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General Aghamaglobulinemia. Hypogammaglobulinemia BDA
D80.2 Election deficit Immunoglobulin A
D80.3 Selective deficit of immunoglobulin g
D80.4 Election deficit Immunoglobulin M
D80.5 Immunodifying Immunoglobulin M
D80.6 Insufficiency of antibodies with close to normal level of immunoglobulins or with hyperimmunoglobulinemia.
Deficiency of antibodies with hyperimmunoglobulinemia
D80.7 Transient Highogamaglobulinemia Children
D80.8 Other immunodeficiency with the predominant defect of antibodies. Capppa-light chain deficiency
D80.9 Immunodeficiency with the predominant defect of antibody unspecified
D81 Combined immunodeficiency
Excluded: Autosomal Recessive Agamaglobulinemia (Swiss Type) (D80.0)
D81.0 Heavy Combined Immunodeficiency with Retic Dysgenesis
D81.1 Heavy Combined Immunodeficiency with Low T- and B-Cells
D81.2 Heavy Combined Immunodeficiency with Low or Normal B-Cell Content
D81.3 Deficity of adenosine formation
D81.5 The deficiency of purrunucleosidephosphorylase
D81.6 Laptop of class I molecules of the main histocompatibility complex. Syndrome "Nude lymphocytes"
D81.7 Laptop Molecules of Class II main histocompatibility complex
D81.8 Other combined immunodeficiency. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency is unspecified. Heavy Combined Imundage Upholstery BDU
D82 Immunodeficiency associated with other significant defects
Excluded: Atthantic Teleangectasia [Louis Bar] (G11.3)
D82.0 Wiscott-Oldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di George syndrome. Syndrome diverticula pharynges.
Aplasia or hypoplasia with immune failure
D82.2 Immunodeficiency with dwarfship due to short limbs
D82.3 Immunodeficiency due to hereditary defect caused by the Epstein-Barr virus.
Captured with X-chromosome lymphoproliferative disease
D82.4 Hyperimmunoglobulin E Syndrome
D82.8 Immunodeficiency associated with other refined significant defects
D82.9 Immunodeficiency associated with a significant defect, unspecified
D83 Normal Variable Immunodeficiency
D83.0 Common variable immunodeficiency with predominant deviations in the amount and functional activity of B-cells
D83.1 Common Variable Immunodeficiency with the predominance of impairment of immunoregulatory T-cells
D83.2 Common Variable Immunodeficiency with Autoantales to B- or T-Cells
D83.8 Other common variable immunodeficiency
D83.9 Common Variable Immunodeficiency Unclean
D84 Other Immunodeficiencies
D84.0 Defect functional antigen-1 lymphocytes
D84.1 Defect in the complement system. Esterase Inhibitor C1 deficiency
D84.8 Other updated immunodeficiency violations
D84.9 Immunodeficiency is uncomfortable
D86 sarcoidosis
D86.1 Sarcoidosis of lymphatic nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of lymph nodes
D86.8 Sarcoidosis of other updated and combined localizations. Iridocyclic with sarcoidosis (H22.1).
Multiple paralysis of clerk nerves during sarcoidosis (G53.2)
Investigating fever [Herford's disease]
D86.9 Sarcoidosis uncomfortable
D89 Other disorders with the involvement of the immune mechanism, not classified in other categories
Excluded: Hyperglobulinemia BDU (R77.1)
monoclonal gammapaty (D47.2)
sustice and transplant rejection (T86 -)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purple. Polyclonal gammapathy BDA
D89.2 hypergammaglobulinemia uncomfortable
D89.8 Other refined violations with the involvement of the immune mechanism not classified in other categories
D89.9 Violation involving the immune mechanism is unspecified. Immune disease BDA
Aplastic and other anemia (D60-D64)
Excelves: Refractory anemia:
- BDA (D46.4)
- with an excess of 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 Review (ICD-10) adopted as a single regulatory document for accounting for incidence, the reasons for the appeals of the population in medical institutions All departments, causes of death.
The ICD-10 has been introduced into the practice of health throughout the territory of the Russian Federation in 1999 by order of the Ministry of Health of Russia from 27.05.97. №170
A new revision (ICD-11) is planned to be planned in 2017 2018.
With changes and additions to WHO.
Processing and transferring changes © MKB-10.com
Postghemorrhagic anemia
Postghemorrhagic anemia is a disease that is accompanied by a decrease in the number of erythrocytes and the concentration of hemoglobin due to massive acute bleeding or as a result of even minor, but chronic blood loss.
Hemoglobin - the protein complex of the erythrocyte, which includes iron. The main function is to transfer oxygen with blood current to all without exception to organs and tissues. If this process is violating this process, quite serious changes begin, which is determined by etiology and the degree of severity of anemia.
Depending on the root causes and the flow of postgemorrhagic anemia distinguish with sharp and chronic forms. In accordance with the international classification system, the disease is divided in this way:
- Secondary iron deficiency anemia after blood loss. Code of ICD 10 D.50
- Acute postgemorrhagic anemia. Code on ICD 10 D.62.
- Congenital anemia after bleeding in the fetus - P61.3.
IN clinical practice Secondary iron deficiency anemia is also called postgemorrhagic chronic anemia.
Causes of acute form of the disease
The main reason for the development of acute postgemorrhagic anemia is the loss of a large amount of blood for a small period of time, which happened as a result:
- Injuries that caused damage to the main arteries.
- Damage to large blood vessels during surgery.
- Razming the uterine tube in the development of ectopic pregnancy.
- Diseases internal organs (most often light, kidneys, heart, gastrointestinal tract), which can lead to acute massive internal bleeding.
In young children, the causes of acute postghemorrhagic anemia are most often injuries of umbilical bodies, congenital pathologies of blood system, damage to the placenta during the cesarean section, early detachment of the placenta, its presence, generic injury.
Causes of the chronic course of postgemorrhagic anemia
Chronic postgemorgic anemia develops as a result of small but regular bleeding. They can appear as a result:
- Hemorrhoid, which is accompanied by the cracks of the rectum by the appearance of blood impurities in the wheel masses.
- Ulcery disease of the stomach and duodenum.
- Abundant menstruation, uterine bleeding against the background of receiving hormonal drugs.
- Beware of vessels with tumor cells.
- Chronic nose bleeding.
- Minor chronic bloodstures in cancer.
- Frequent blood fences, installation of catheters and other similar manipulations.
- Heavy kidney diseases with blood excretion with urine.
- Invasia Helminti.
- Cirrhosis of the liver, chronic liver failure.
Cause chronic anemia Gemorrhagic diathesis can also be similar. This is a group of diseases in which a person has a tendency to bleeding due to the violation of homeostasis.
Symptoms and blood pattern with anemia as a result of acute blood loss
Clinical picture Acute postgymorrhagic anemia develops very quickly. The main symptoms of this disease join the manifestations of general shock as a result of acute bleeding. In general, observed:
- Reduced blood pressure.
- Castle or loss of consciousness.
- Strong pallor, a bluish shade of nasolabial fold.
- Fit-shaped pulse.
- Vomiting.
- Increased sweating, and the so-called cold sweat is observed.
- Chills.
- Cramps.
If the bleeding was successfully stopped, such symptoms are replaced by dizziness, noise in the ears, loss of orientation, violation of vision, shortness, sickness of heartbeat rhythm. The pallor of the skin and mucous membranes, reduced blood pressure remains preserved.
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Iron-deficiency anemia. Symptoms, features and methods �
Anemia is one of the most frequent causes
Changes in blood test results for several days after the binding and the development of anemia are closely related to compensation mechanisms that are "included" in the body in response to the loss of a large blood volume. They can be divided into such stages:
- The reflex phase that develops on the first day after blood loss. The redistribution and centralization of blood circulation begins, the peripheral resistance of the vessels increases. In this case, there is a decrease in the number of erythrocytes at normal values \u200b\u200bof the concentration of hemoglobin and hematocrit.
- The hydrama phase proceeds from the second to the fourth day. The extracellular fluid falls into the vessels, glycogenolysis is activated in the liver, which leads to an increase in the content of glucose. Gradually, symptoms of anemia appear in the blood pattern: the hemoglobin concentration decreases, hematocrit decreases. However, the value of the color indicator still remains normal. Due to the activation of thrombosis processes, the amount of platelets decreases, and due to the loss of leukocytes during bleeding, leukopenia is observed.
- The bone marrow phase begins from the fifth day after bleeding. Insufficient supply of organs and tissues with oxygen activates blood formation processes. In addition to low hemoglobin, hematocrit, tomb cell and leukopenia at this stage, there is a decrease in the total number of erythrocytes. In the study of blood smear, there is a presence of young form of erythrocytes: reticulocytes, sometimes erythroblasts.
Similar changes in the blood pattern are described in many situational tasks for future doctors.
Symptoms and diagnosis of anemia in chronic bleeding
Chronic postgemorrhagic anemia is similar to iron deficiency in its symptoms, since regular mile bleeding leads to the deficiency of this trace element. The flow of this blood disease depends on the degree of its severity. It is determined depending on the concentration of hemoglobin. Normally, men are 135 - 160 g / l, and in women 120 - 140 g / l. In children, this value varies depending on age from 200 in babies up to 150 in adolescents.
The degree of postgemorrhagic chronic anemia is the concentration of hemoglobin
- 1 (Easy) degree 90 - 110 g / l
- 2 degree (moderate severity) 70 - 90 g / l
- 3 degree (heavy) below 70 g / l
At the initial stage of the development of the disease, patients make complaints about light dizziness, flickering "flies" before their eyes, increased fatigue. Externally noted the pallor of the skin and mucous membranes.
At the second stage, the listed symptoms add a decrease in appetite, sometimes nausea, diarrhea, or, on the contrary, constipation, shortness of breath. When listening to the heart tones, doctors note characteristic of chronic post-gemorrhagic noise anemia in the heart. Changes the condition of the skin: the skin becomes dry, peel. Painful and inflamed cracks appear in the corners of the mouth. The condition of hair and nails deteriorates.
A severe degree of anemia is manifested by numbness and a sense of tingling in the fingers and legs, specific taste addiction appear, for example, some patients begin to eat chalk, the perception of smells changes. Very often, this stage of chronic postgemorrhagic anemia is accompanied by fast-horror caries, stomatitis.
The diagnosis of postgemorrhagic anemia is based on the results of clinical analysis of blood. In addition to the decline in hemoglobin and red blood cells characteristic of all types of anemia, a decrease in the color indicator is revealed. Its value varies in the range of 0.5 - 0.6. In addition, when chronic postgemorrhagic anemia, modified erythrocytes (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 impose a harness, a gulling bandage and deliver the victim to the hospital. Above the inner bleeding, in addition to pallor, cyanosis and the perishes of consciousness indicates severe dryness in the mouth. At home to assist a person in such a state is impossible, so stop internal bleeding It is carried out only in the hospital.
After detecting the source and stop the bleeding, it is necessary to restore the blood sole blars in urgency. Reopolyglyukin, hemodez, polyglyukine are prescribed for this. Ostly blood loss is also compensated for blood transfusions, taking into account the compatibility of the rees-factor and blood group. The volume of hemotransphus is usually 400 - 500 ml. These activities should be carried out very quickly, since the rapid loss even the ¼ total blood can lead to a fatal outcome.
After stopping the state of the shock and carrying out all the necessary manipulations, they move to standard treatment, which is to introduce iron and enhanced nutrition to replenish the deficit of vitamins and microelements. Usually prescribed Ferrorum Lek, Faltum, Malto.
Typically, the restoration of a normal blood pattern occurs after 6 - 8 weeks, but the use of drugs to normalize the blood formation continues to six months.
Treatment of chronic postgemorrhagic anemia
The first and most important stage in the treatment of postgemorrhagic chronic anemia is to determine the source of bleeding and its elimination. Even a loss of 10 - 15 ml of blood per day deprives the body of the entire amount of iron that has entered this day with food.
A comprehensive examination of the patient is carried out, which is mandatory involving consultations of a gastroenterologist, a proctologist, hematologist, a gynecologist for women, endocrinologist. After identifying the disease, which caused the development of chronic postgemorrhagic anemia, the treatment immediately begin.
In parallel, drugs are prescribed, which contain iron. For adults, his daily dose is about 100-10 mg. Appointed comprehensive meanswhich in addition to iron contain ascorbic acid and vitamins of group B, which contributes to its better absorption. This is sorbifer Durules, Ferroplex, Feneuls.
For severe course Postghemorrhagic chronic anemia for stimulating blood flow processes shows the transfusion of the erythrocyte mass and injecting administration of medicines with iron. Prescribed Ferlamm, Malto, Licferre and similar medicines.
Recovery after the main course of treatment
The duration of receiving iron-containing drugs determines the doctor. In addition to the use of various drugs to restore the normal supply of oxygen organs and replenishing iron reserves in the body, full-fledged nutrition.
In the diet of a person who suffered posthemorrhagic anemia, the proteins and iron should be present in obligatory. Preference should be given to meat, eggs, equality products. The leaders in the content of iron are meat offal, especially the beef liver, meat, fish, caviar, legumes, nuts, buckwheat and oatmeal.
When drawing a diet, attention should be paid not only to how much iron contains one or another product, but also to the degree of its suction in the body. It increases with the use of vegetables and fruits, which contain vitamins B and C. These are citrus, black currant, raspberry, etc.
Current and therapy of posthemorrhagic anemia in children
Postgemorrhagic anemia in children proceeds much harder, especially sharp her form. The clinical picture of this pathology is practically no different from the adult, but develops faster. And if an adult has a certain amount of blood lost blood compensated protective reactions The body, then the child can lead to a fatal outcome.
Treatment of acute and chronic form of postgymorrhagic anemia in children is the same. After identifying the cause and elimination of bleeding, the transfusion of the erythrocyte mass is prescribed at the rate of 10 - 15 ml per kg of weight, gland preparations. Their dosage is calculated individually depending on the severity of the anemia and the state of the child.
Children at the age of about six months are recommended early introduction of dust, and it should be started with products with a high content of iron. Breasts show the transition to special vitaminized mixtures. If the disease, which led to the development of postgemorrhagic anemia, is chronic and is not amenable to treatment, the preventive courses of iron preparations must be repeated regularly.
With timely, the beginning of the treatment and non-critical blood loss, the forecast is generally favorable. After compensating for iron deficiency, the child quickly goes on the amendment.
Anemia - This is the inconsistency of the proportion of hemoglobin in human blood to the criteria adopted by the World Health Organization for a specific age and gender. The term "anemia" is not a diagnosis of the disease, and only indicates abnormal changes in blood test.
Code on the international classification of diseases of the ICD-10: iron deficiency anemia - D50.
The most common anemia as a result of blood loss and iron deficiency anemia:
- Anemia as a result of blood loss may be caused by long menstruation, bleeding in the digestive tract and urinary trait, injury, operations, oncological diseases.
- Iron-deficiency anemia It is formed as a result of the deficit in the production of the organism of red blood cells
Causes and factors
Among the factors that increase the risk of sick anemia, doctors identify:
- insufficient use of iron, vitamins and minerals;
- poor nutrition;
- blood loss due to injury or operation;
- kidney disease;
- diabetes;
- rheumatoid arthritis;
- HIV AIDS;
- inflammatory bowel diseases (including crown disease);
- liver diseases;
- heart failure;
- diseases thyroid gland;
- anemia after a disease caused by infection.
The erroneous opinion is that anemia arise only after the disease.
The reasons are much larger:
Degrees and types of anemia
- lungs- the amount of hemoglobin is 90 g / l and higher;
- middle severity - hemoglobin 70-90 g / l;
- heavy Anemia - hemoglobin below 70 g / l at a norm for women 120-140 g / l, for men - 130-160 g / l.
- Anemia due to iron deficiency. Women during pregnancy, menstruation and in the period of iron lactation, it is necessary several times more than usual. Therefore, iron deficiency anemia often happens during this period.
Also also baby body Requires a lot of iron. Such anemia can be treated with iron-containing tablets or syrups. - Megaloblastic anemia Arises as a result of a shortage of thyroid hormones, liver disease and tuberculosis. This type of anemia caused by a disadvantage of vitamin B12 and folic acid. Early diagnosis and treatment are very important for patients with megaloblastic anemia.
Weakness, fatigue, numbness of the hands, pain and burning language, the sword is common complaints of this type of disease. - Chronic infectious anemia It occurs due to a lack of bone marrow, with tuberculosis, leukemia and as a result of the reception of some drugs, which contains toxic substances.
- Mediterranean anemia (The disease, also known as thalassemia) is a hereditary blood disease. High incidence of this type is observed in Italians and Greeks. At the initial stage, the symptoms are the same as with anemia due to iron deficiency.
As disease progressing Jaundice is observed, anemia is added as a result of kidney disease and spleen growth. Thalassemia is treated with blood transfusion. - Sickle-cell anemia This is also hereditary disease in which the structure of hemoglobin in the blood differs from normal indicators. The erythrocyte takes the shape of the crescent, the time of his life is very short. This type is observed in the representatives of the Black Race. The carrier of the gene of this anemia is women.
- Aplastic anemia This is a violation of the production of red blood cells in the bone marrow. The cause can be evaporation harmful substances, such as benzene, arsenic, exposure to radiation. The level of blood cells of platelets is also reduced.
The opposite of aplastic anemia is polycythemia, during which the usual number of blood red blood cells increases more than 2 times. The patient's skin becomes red and an increase in blood pressure can be observed. The reason for this is the lack of oxygen. This disease is treated by removing blood from the human body.
Who can get anemia?
Anemia is a disease that affects all age and ethnic groups, races.
- Some children in the first year of life The anemia is at risk due to iron deficiency. This is prematurely born and children who fed breast milk With a lack of iron. Such babies anemia develops during the first 6 months.
- Children from one to two years are subject to the development of anemia. Especially if they drink a lot of cow's milk and do not eat food with a sufficient amount of iron. As part of cow milk, there is no sufficient volume of iron for the growth of the child. Instead of milk Toddler under 3 years old should be fed with rich glands. Cow's milk can also prevent iron absorption in the body.
- Researchers continue to learn As anemia affects adults. More than ten percent of adults are constantly in a state of light anemia. Most of these people have other medical diagnoses.
Signs and symptoms
The most frequent symptom of anemia is fatigue. People feel tired and exhausted.
Other features and symptoms of anemia include:
- difficulty breathing;
- dizziness;
- headaches;
- cold feet and palm;
- chest pain.
These symptoms may occur due to the fact that the heart has become heavier to punish the blood in the body rich in oxygen.
In mild I. middle degree anemia (iron deficiency) symptoms are:
- desire to eat a foreign object: earth, ice, limestone, starch;
- cracks in the corners of the mouth;
- annoyed tongue.
Signs of folic acid deficit:
- diarrhea;
- depression;
- swollen and red language;
Symptoms of anemia due to lack of vitamin B12:
- tingling and loss of sensitivity in the upper and lower limbs;
- complexity in distinguishing yellow and blue;
- swelling and pain in the larynx;
- weight loss;
- skin blaracing;
- diarrhea;
- depression;
- reduced intellectual function.
Complications
The doctor when the diagnosis should be prevented than dangerous anemia:
- Patients may have arrhythmia- Problem with speed and rhythm of heart abbreviations. Arrhythmia can lead to damage to the heart and heart failure.
- Anemia can Also lead to damage to other organs in the body: blood cannot provide organs with sufficient oxygen.
- In cancer And HIV / AIDS a disease may weaken the organism, and reduce the result from treatment.
- Elevated risk The emergence of anemia in kidney disease, in patients with heart problems.
- Some types of anemia There are insufficient fluid consumption or excessive water loss in the body. Strong dehydration is the cause of blood disease.
Diagnostics
The doctor must learn the family history of the disease to determine the hereditary or acquired type of illness. He can ask a patient about the general signs of anemia, whether he is on a diet.
The physical examination is:
- listening to the rhythm of the heart and the regularity of breathing;
- measuring the size of the spleen;
- the presence of pelvic or rectal bleeding.
- laboratory tests will help determine the type of anemia:
- general blood analysis;
- hemograms.
The hemogram test measures the hemoglobin value and blood hematocrit. Low hemoglobin and hematocrit is a sign of anemia. Normal values \u200b\u200bvary depending on race and population.
Other tests and procedures:
- Gemoglobin electrophoresis Determines the number different types Hemoglobin in the blood.
- Measurement of reticulocyte - This is the count of young red blood tauros in the blood. This test shows the rate of production of erythrocyte bone marrow.
- Tests for measuring iron in the blood - This is determining the level and general content of iron, transmission, binding blood ability.
- If the doctor suspects anemia because of blood lossHe can offer an analysis to determine the source of bleeding. Suggested to pass the analysis of the feces on the definition of blood in the chair.
If there is blood, endoscopy is needed: Examination of the inside of the digestive system with a small camera. - May need Also analysis of bone marrow.
How is anemia treat?
The treatment of anemia depends on the cause, gravity and type of illness. The purpose of treatment is an increase in oxygen in the blood by reproduction of red cells and increase the level of hemoglobin.
Hemoglobin is a protein that transports oxygen to the body with iron.
Changes and supplement power supply
Iron
The body needs hardware for the formation of hemoglobin. The body absorbs iron from meat easier than from vegetables and other foods. For the treatment of anemia, there is more meat, especially red (beef or liver), as well as chicken, turkey and seafood.
In addition to meat, Iron is in:
Vitamin B12.
Low vitamin B12 can lead to malignant anemia.
The sources of vitamin B12 are:
- grain;
- red meat, liver, bird, fish;
- eggs and dairy products (milk, yogurt and cheese);
- vegetable iron-based drinks and vegetarian products enriched with vitamin B12.
Folic acid
The body needs folic acid to produce new cells and protect them. Folic acid is necessary for pregnant women. She protects against anemia and helps healthy fetus development.
A good source of folic acid food is:
- bread, pasta, rice;
- spinach, dark green leafy vegetables;
- dry beans;
- liver;
- eggs;
- bananas, oranges, orange juice and some other fruits and juices.
Vitamin C
It helps the body to absorb iron. Fruits and vegetables, especially citrus, is a good source of vitamin C. In fresh and frozen fruits and vegetables, more vitamin C than in canned products.
Vitamin C is rich in kiwi, strawberries, melons, broccoli, pepper, brussels sprouts, Tomatoes, potatoes, spinach, radishes.
Medications
The doctor may prescribe medications for the treatment of the main cause of anemia and increasing the number of red blood cells in the body.
It can be:
- antibiotics for the treatment of infections;
- hormones to prevent excessive menstrual bleeding in young girls and women;
- artificial erythropoietin for stimulating erythrocyte production.
Operations
If anemia has grown into a heavy stage, an operation may be required: transplantation of blood stem cells and bone marrow, blood transfusion.
Stem cell transplantation is carried out to replace damaged in the patient from another healthy donor. Stem cells are in the bone marrow. Cell transmission is carried out through the tube inserted into the breast vein. The process is similar to blood transfusion.
Surgical interventions
With threatening life bleeding in the body causing anemia, surgical intervention is necessary.
For example, anemia for ulcerative ulcer of stomach or colon cancer require surgical intervention to prevent bleeding.
Prevention
Some types of anemia can be prevented by eating food rich with iron and vitamins. Useful to take nutritional supplements during a diet.
Important! For women who are fond of weight loss and various diets, the reception of additional additives with iron and vitamin complexes is mandatory!
After the main treatment of anemia, it is necessary to maintain contact with your attending physician and regularly check the composition of the blood.
If the patient inherited a malignant type of anemia, treatment and prevention should last for years. To this you need to be prepared.
Anemia in children and young people
Chronic diseases, iron deficiency and poor nutrition can lead to anemia. Diseases are often accompanied by other health problems. Thus, signs and symptoms of anemia are often not so obvious.
Be sure to consult a doctor if symptoms of anemia or a person are on a diet. It is possible to need blood transfusion or hormonal therapy. If you diagnose anemia on time, it can be fully cured.
Anemia is one of the most common blood diseases, both among the adult and among the children's population.
For registration medical documentation Patient with anemia of any etiology, the doctor uses the anemia code for the ICD 10. There are different forms of the disease, depending on the cause, which led to a decrease in hemoglobin and red blood cells in the blood. Anemia can be iron deficiency, folic-deficient, B-12 scarce, hemolytic, aplastic and unspecified.
Causes of the occurrence, clinic and treatment of pathological conditions
The overall development mechanism for any type of illness is the violation of the work of the hematopoietic organs due to chronic lack of certain nutrients or, in some cases, due to the rapid destruction of blood cells in the bloodstream. An important role is also played by immune disorders, the effects of toxic substances.
In the ICD 10 anemia refers to the class of blood disease and it has a cipher D50-D64.
The main clinical symptoms are:
- weakness;
- pallor;
- dizziness;
- pathological changes in taste;
- pathological changes in skin cover;
- headache;
- digestive problems;
- inxication (with hemolytic forms).
Treatment is carried out depending on the cause pathological decline Hemoglobin and red blood cells. Be sure to choose the correct diet and the mode for the patient. Anemia uncomfortable requires an expanded comprehensive examination of the patient's body and symptomatic treatment at the initial stages.
Among various anemics conductible anemiathey are the most common and amount to about 80% of all anemia.
Iron-deficiency anemia- hypochromic microcolitical anemia, developing due to an absolute decrease in iron reserves in the body. Conducting anemia arises, as a rule, with chronic loss of blood or insufficient intake of iron into the body.
According to the World Health Organization, each 3rd woman and every 6th man in the world (200 million people) suffer from iron deficiency anemia.
Mechanism exchange
Iron is an indispensable biometallom, which plays an important role in the functioning of cells of many organism systems. The biological value of iron is determined by its ability to reversibly oxidize and restore. This property ensures the participation of iron in the process of tissue respiration. Iron is only 0.0065% of body weight. In the body of a man with a body weight of 70 kg, it contains approximately 3.5 g (50 mg / kg of body weight) of iron. The iron content in the body of a woman with a mass of body 60 kg is approximately 2.1 g (35 mg / kg body weight). The iron compounds have a different structure, have characteristic only for them with functional activity and play an important biological role. The most important iron-containing compounds include: hemoprotein, the structural component of which is gem (hemoglobin, mioglobin, cytochrome, catalase, peroxidase), the enzymes of the unhealthy group (succinate dehydrogenase, acetyl-co-dehydrogenase, xantinoxidase), ferritin, hemosiderin, transferin. The iron is included in the complex compounds and distributed in the body as follows:
- gem iron - 70%;
- Iron depot - 18% (intracellular accumulation in the form of ferritin and hemosiderin);
- functioning iron - 12% (moglobin and containing iron enzymes);
- Transported iron - 0.1% (iron associated with transferin).
There are two types of iron: gem and nonsense. Ham iron is part of hemoglobin. It is contained only in a small part of the edible diet (meat products), is well absorbed (by 20-30%), other components of food practically do not affect its absorption. The non-migrant iron is in a free ionic form - bivalent (Fe II) or trivalent iron (Fe III). Most of the edible iron is non-flag (contained mainly in vegetables). The degree of assimilation is lower than hemovoy, and depends on a number of factors. Only bivalent non-brass iron is absorbed from food products. To "turn" trivalent iron into a divalent, a reducing agent is needed, the role of which in most cases ascorbic acid is played (vitamin C). In the process of suction in the intestinal mucosa cells, Zakis iron FE2 + is converted into oxide FE3 + and is associated with a special carrier protein - transferrin, which carries out the transport of iron to hematopoietic tissues and iron deposit places.
Iron accumulation is carried out by ferritin and hemosiderin proteins. If necessary, iron can be actively released from ferritin and used for erythropoese. Hemosiderine is a derivative of ferritin with a higher iron content. From hemosiderery iron is released slowly. Beginning (Prelatented) Iron deficiency can be determined at a reduced concentration of ferritin before the exhaustion of iron reserves, with a still continuous normal concentration of iron and transferin in serum.
What provokes iron deficiency anemia:
The main etiopathogenetic factor in the development of iron deficiency anemia is a deficiency of iron. The most frequent causes of the emergence of iron deficiency states are:
1. Losses of iron in chronic bleeding (most frequent causereaching 80%):
- bleeding from the gastrointestinal tract: ulcerative disease, erosive gastritis, varicose expansion of esophagel veins, colon diverticulas, invasion of ankylostomas, tumors, hay, hemorrhoids;
- Long-term I. abundant menstruation, endometriosis, fibromyoma;
- Macro- and Microhematuria: chronic glomerulose and pyelonephritis, urolithiasis disease, polycystic kidney, kidney tumors and bladder;
- nasal, pulmonary bleeding;
- blood loss during hemodialysis;
- uncontrolled donation;
2. Insufficient absorption of iron:
- resection of the small intestine;
- chronic enteritis;
- Malabsorption syndrome;
- intestinal amyloidosis;
3. Increased needle need:
- intense growth;
- Pregnancy;
- period of breastfeeding;
- sports;
4. Insufficient iron intake with food:
- newborn;
-- Small children;
- Vegetarianism.
Pathogenesis (what happens?) During iron deficiency anemia:
The pathogenetic development of the iron deficiency state can be divided into several stages:
1. Prelative iron deficiency (accumulation deficiency) - a decrease in ferritin levels and a decrease in iron content in the bone marrow is increased, iron absorption is increased;
2. Latent iron deficiency (iron-deficient erythropoes) - whey iron is additionally reduced, transferin concentration increases, the content of sideroblasts in the bone marrow decreases;
3. The pronounced deficiency of iron \u003d iron deficiency anemia - the concentration of hemoglobin, erythrocytes and hematocrites is additionally reduced.
Symptoms of iron deficiency anemia:
In the period of hidden iron deficit, many subjective complaints and clinical signs characteristic of iron deficiency anemia appear. Patients celebrate general weakness, malaise, reduced performance. Already during this period there may be a perversion of taste, dryness and discharge of the language, disrupting swallowing with a sensation foreign bodies In the throat, heartbeat, shortness of breath.
With an objective examination of patients, "small iron deficit symptoms" are found: the papillary atrophy of the language, Haylitis, dry skin and hair, nail fragility, burning and itching vulva. All these signs of violation of the trophic epithelial tissues are associated with tissue siderpenia and hypoxia.
Patients with iron deficiency anemia celebrate general weakness, fast fatigue, difficulty in focusing, sometimes drowsiness. Headache appear, dizziness. With severe anemia, fainting is possible. These complaints are usually dependent on the degree of reduction of hemoglobin, but on the duration of the disease and age of patients.
Conducting anemia is also characterized by changes in skin, nails and hair. The skin is usually pale, sometimes with a slight greenish tint (chlorosis) and with an easily arising brush cheek, it becomes dry, flabby, flakes, cracks are easily formed. Hair is losing glitter, gray, thinned, easily break, they are thin and seed early. Specified nail changes: they become thin, frosted, flattened, easily relax and break, it appears. With pronounced changes, the nails acquire a concave, fabulous form (coyloniching). In patients with iron deficiency anemia, muscle weakness occurs, which is not observed with other types of anemia. It is referred to the manifestations of tissue siderpiest. Atrophic changes occur in the mucous membranes of the digestive channel, respiratory organs, genitals. The damage to the mucous membrane of the digestive channel is a typical sign of iron deficiency states.
There is a decrease in appetite. There is a need for acidic, acute, salted food. In more severe cases, smell perversion, taste (Pica Chlorotica) are observed: eating chalk, lime, raw croup, pogophagia (attraction to ice use). Signs of tissue siderpoints quickly disappear after taking iron preparations.
Diagnosis of iron deficiency anemia:
Maintenance laboratory Laboratory Diagnostics Labor Normianext:
1. The average hemoglobin content in erythrocyte in picograms (the norm 27-35 pg) is reduced. To calculate it, the color indicator is multiplied by 33.3. For example, in a color indicator of 0.7 x 33.3, the hemoglobin content is 23.3 pg.
2. The average hemoglobin concentration in erythrocyte is reduced; Normally, it is 31-36 g / dl.
3. The hypochromy of red blood cells is determined by microscopy of the smear of peripheral blood and is characterized by an increase in the central enlightenment zone in the erythrocyte; Normally, the ratio of central enlightenment to peripheral dimension is 1: 1; With iron deficiency anemia - 2 + 3: 1.
4. Microcytosis of erythrocytes - decrease in their size.
5. Miscellaneous intensity of red blood cells - anisochromia; The presence of both hypo- and normo-chromium erythrocytes.
6. Different form Erythrocytes - Poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and the period of therapy) during iron deficiency anemia remains normal.
8. The content of leukocytes is also within the normal range (except in cases of blood loss or oncopathology).
9. The platelet content is more commonly within the normal range; Moderate thrombocytosis is possible with blood loss at the time of the examination, and the platelet content decreases, when the iron-leveling is based on blood-deficiency anemia due to thrombocytopenia (for example, in DVS syndrome, Verlgood disease).
10. Reducing the number of siderocytes down to their disappearance (Siderocyte is an erythrocyte containing iron granules). In order to standardize the manufacture of peripheral blood smears, it is recommended to use special automatic devices; Forming monolayer cells improves the quality of their identification.
Blood chemistry:
1. Reducing iron content in blood serum (normally in men 13-30 μmol / l, in women 12-25 μmol / l).
2. The RUNs are increased (reflects the amount of iron that can be due to free transferin; RUB is normal - 30-86 μmol / l).
3. The study of transferrin receptors by the immununimal method; their level is increased in patients with iron deficiency anemia (in patients with anemia chronic diseases - Normally or reduced, despite similar indicators of iron exchange.
4. Latent iron binding ability of blood serum is increased (determined by subtracting from the indicators of the root iron content of the serum iron).
5. Percentage of transferlic rope saturation (the ratio of the iron of the blood serum to the RUB; normally 16-50%) is reduced.
6. The level of serum ferritin is also reduced (normally 15-150 μg / l).
At the same time, in patients with iron deficiency anemia, the number of transferrrin receptors was increased and the level of erythropoietin in blood serum (blood-formation compensatory reactions) was increased. The volume of erythropoietin secretion is inversely proportional to the size of the oxygen-speaking capacity of blood and is directly proportional to the oxygen request of the blood. It should be borne in mind that the level of serum iron is higher in the morning hours; Before starting and during menstruation, it is higher than after menstruation. The content of iron in the serum in the first weeks of pregnancy is higher than in its last trimester. The level of serum iron rises on the 2nd-4th day after treatment iron-containing drugsand then decreases. Significant consumption of meat products on the eve of the study is accompanied by hypersidermia. These data must be considered when evaluating the results of the serum iron research. It is equally important to comply with the technique of a laboratory study, blood collection rules. Thus, the test tubes in which blood collects must first be washed with hydrochloric acid and bidistalized water.
Research myelogramreselects a moderate normurelastic reaction and a sharp decrease in the content of sideroblasts (erythrocarocytes containing iron granules).
On the reserves of iron in the body are judged by the results of the desperial sample. W. healthy man after intravenous administration 500 mg of the desferla is derived from 0.8 to 1.2 mg of iron, while the patient with iron deficiency anemia is reduced to 0.2 mg in a patient with iron deficiency anemia. New domestic drug Deferikolixam is identical to the doctor, but it circulates longer in the blood and therefore more precisely reflects the level of iron reserves in the body.
Given the level of hemoglobin, iron deficiency anemia, like other forms of anemia, are divided into anemia of severe, medium and easy degree. With iron deficiency anemia, the concentration of hemoglobin is below the norm, but more than 90 g / l; with iron deficiency anemia of the average degree of hemoglobin content of less than 90 g / l, but more than 70 g / l; With a severe degree of iron deficiency anemia, the concentration of hemoglobin is less than 70 g / l. At the same time, clinical signs of the severity of anemia (symptoms of hypoxic nature) do not always correspond to the severity of anemia under laboratory criteria. Therefore, the classification of anemia by the severity of clinical symptoms is proposed.
For clinical manifestations, 5 degrees of the severity of anemia are distinguished:
1. Anemia without clinical manifestations;
2. Anemic syndrome of moderate severity;
3. pronounced anemic syndrome;
4. anemic prema;
5. Anemic Coma.
Moderate severity of anemia is characterized total weakness, specific features (for example, sider-poenic or signs of vitamin B12 deficiency); With a pronounced severity of the anemia, heartbeat appear, shortness of breath, dizziness, etc. Premate and comatose state can develop in a matter of hours, which is especially characteristic of megaloblastic anemia.
Modern clinical studies show that laboratory and clinical heterogeneity are observed among patients with iron deficiency anemia. So, in part of patients with signs of iron deficiency anemia and accompanying inflammatory and infectious diseases The level of serum and erythrocyte ferritin is not reduced, however, after eliminating the exacerbation of the underlying disease, their content falls, which indicates the activation of macrophages in the process of iron spending. Part of the patients, the level of erythrocyte ferritin even increases, especially in patients with a long flow of iron deficiency anemia, which leads to ineffective erythropoosis. Sometimes there is an increase in the level of serum iron and erythrocyte ferritin, a decrease in transferrine of blood serum. It is assumed that in these cases the process of transferring iron to hexintezing cells is disturbed. In some cases, iron deficiency, vitamin B12 and folic acid is determined simultaneously.
Thus, even the level of serum iron does not always reflect the degree of iron deficiency in the body in the presence of other signs of iron deficiency anemia. Only the level of the RUB in iron deficiency anemia is always increased. Therefore, no biochemical indicator, incl. OZHSS, one cannot be considered as an absolute diagnostic criterion for iron deficiency anemia. At the same time, the morphological characteristics of peripheral blood erythrocytes and computer analysis of the basic parameters of the erythrocytes are decisive in screening diagnostics of iron deficiency anemia.
The diagnosis of iron deficiency conditions is hampered in cases where the hemoglobin content remains normal. Iron deficiency anemia develops with the same risk factors as under iron deficiency anemia, as well as in persons with an increased physiological need for iron, primarily premature children in early age, adolescents with a rapid increase in the growth and body weight, in blood donors, with an alimentary dystrophy. In the first stage of iron deficiency clinical manifestations There are no, and iron deficiency is determined by the content of hemosiderin in bone marrow macrophages and on the absorption of radioactive iron in the gastrointestinal tract. In the second stage (latent iron deficiency) there is an increase in the concentration of protoporphyrin in red blood cells, the number of sideroblasts decreases, morphological signs (microcitosis, erythrocyte hypochromy) appear, the average content and concentration of hemoglobin in red blood cells decreases, the level of serum and erythrocyte ferritin is reduced, the saturation of transferry iron is reduced. The level of hemoglobin in this stage remains high enough, and clinical signs are characterized by a decrease in tolerance to exercise. The third stage is manifested by obvious clinical and laboratory signs of anemia.
Survey of patients with iron deficiency anemia
To eliminate anemia with common features with iron deficiency anemia, and the identification of the cause of iron deficiency is necessary complete clinical examination of the patient:
General blood analysiswith the obligatory determination of the number of platelets, reticulocytes, the study of the morphology of the erythrocytes.
Blood chemistry:determination of iron levels, yazss, ferritin, bilirubin (associated and free), hemoglobin.
In all cases it is necessary explore the bone marrowbefore the appointment of vitamin B12 (first of all, for differential diagnosis with megaloblastic anemia).
To identify the cause of iron deficiency anemia, women require a preliminary consultation of the gynecologist to eliminate the diseases of the uterus and its appendages, and men include a proctologist to eliminate bleeding hemorrhoids and a urologist to eliminate the pathology of the prostate gland.
There are cases of extractive endometriosis, for example in respiratory tract. In these cases, heloching is observed; Fibrobronchoscopy with histological examination of the bioptack of the mucous membrane of the bronchi allows you to diagnose.
The survey plan also includes x-ray and endoscopic study of the stomach and intestines in order to exclude ulcers, tumors, incl. Glometic, as well as polyps, diverticulous, crown disease, ulcerative colitis, etc. In suspected pulmonary siderosis, radiography and tomography of the lungs are carried out, the study of sputum on alveolar macrophages containing hemosidemin; In rare cases, histological examination of the lung biopsy is necessary. If the kidney pathology is suggested, a common urine analysis is needed, the study of blood serum on urea and creatinine, according to the testimony - ultrasonic and X-ray examination of the kidneys. In some cases, it is necessary to exclude endocrine pathology: a mixture, in which iron deficiency can develop secondly due to the decent damage; Rheumatic polymalgia - rare disease connective tissue The elderly women (less often - in men), characterized by pain in the muscles of the shoulder or pelvic belt without any objective changes in them, and in the analysis of blood - anemia and an increase in ESO.
Differential diagnostics of iron deficiency anemia
When diagnosing iron deficiency anemia must be carried out differential diagnosis with other hypochromic anemia.
Tableological operational anemia is quite frequent pathology and in terms of development ranks second among all anemia (after iron deficiency anemia). It develops with acute and chronic infectious inflammatory diseases, sepsis, tuberculosis, rheumatoid arthritis, liver diseases, oncological diseases, IBS, etc. The mechanism of development of hypochromic anemia under these states is associated with the redistribution of iron in the body (it is mainly in the depot) and violation Mechanism of recycling iron from the depot. With the above diseases, the macrophageal system is activated when macrophages under the activation conditions are firmly held by iron, thereby disrupting the process of its reutelation. IN general Analysis{!LANG-8f9f77759f12ffb43c2101d3182a0380!}<80 г/л).
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