Chronic posthemorrhagic anemia ICD code 10. Posthemorrhagic anemia

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

Excluded: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine diseases, nutritional and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), trauma, poisoning and certain other consequences of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)

This class contains the following blocks:

D50-D53 Anemia associated with nutrition

D55-D59 Hemolytic anemias

D60-D64 Aplastic and other anemias

D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions

D70-D77 Other diseases of the blood and hematopoietic organs

D80-D89 Selected disorders involving the immune mechanism

The following categories are marked with an asterisk:

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

NUTRITION-RELATED ANEMIA (D50-D53)

D50 Iron deficiency anemia

D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.

Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)

D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson syndrome

D50.8 Other iron deficiency anemias

D50.9 Iron deficiency anemia, unspecified

D51 Vitamin B12 deficiency anemia

Excludes: vitamin B12 deficiency (E53.8)

D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.

Congenital intrinsic factor deficiency

D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.

Imerslund(-Gresbeck) syndrome. Megaloblastic hereditary anemia

D51.2 Transcobalamin II deficiency

D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Anemia of vegetarians

D51.8 Other vitamin B12 deficiency anemias

D51.9 Vitamin B12 deficiency anemia, unspecified

D52 Folate deficiency anemia

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

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

use an additional external cause code (class XX)

D52.8 Other folate deficiency anemias

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

D53 Other diet-related anemias

Includes: megaloblastic anemia not responding to vitamin therapy

nom B12 or folate

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

Excludes: Lesch-Nychen syndrome (E79.1)

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

Excludes: DiGuglielmo disease (C94.0)

D53.2 Anemia due to scurvy.

Excludes: scurvy (E54)

D53.8 Other specified anemias associated with nutrition.

Anemia associated with deficiency:

Excludes: malnutrition without mention of

anemia, such as:

Copper deficiency (E61.0)

Molybdenum deficiency (E61.5)

Zinc deficiency (E60)

D53.9 Diet-related anemia, unspecified. Simple chronic anemia.

Excludes: anemia NOS (D64.9)

HEMOLYTIC ANEMIA (D55-D59)

D55 Anemia due to enzyme disorders

Excludes: drug-induced enzyme deficiency anemia (D59.2)

D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6-PD deficiency anemia

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

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

bypass of the metabolic pathway. Hemolytic nonspherocytic anemia (hereditary) type 1

D55.2 Anemia due to disorders of glycolytic enzymes.

Hemolytic non-spherocytic (hereditary) type II

Due to hexokinase deficiency

Due to pyruvate kinase deficiency

Due to triosephosphate isomerase deficiency

D55.3 Anemia due to disorders of nucleotide metabolism

D55.8 Other anemia due to enzyme disorders

D55.9 Anemia due to enzyme disorder, unspecified

D56 Thalassemia

Excludes: hydrops fetalis due to hemolytic disease (P56.-)

D56.1 Beta thalassemia. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.

D56.3 Carriage of thalassemia trait

D56.4 Hereditary persistence of fetal hemoglobin [HFH]

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

Thalassemia minor (mixed) (with other hemoglobinopathy)

D57 Sickle cell disorders

Excludes: other hemoglobinopathies (D58. -)

sickle cell beta thalassemia (D56.1)

D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis

D57.1 Sickle cell anemia without crisis.

D57.2 Double heterozygous sickle cell disorders

D57.3 Carriage of the sickle cell trait. Carriage of hemoglobin S. Heterozygous hemoglobin S

D57.8 Other sickle cell disorders

D58 Other hereditary hemolytic anemias

D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.

Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome

D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)

D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.

Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.

Excludes: familial polycythemia (D75.0)

Hb-M disease (D74.0)

hereditary persistence of fetal hemoglobin (D56.4)

altitude-related polycythemia (D75.1)

D58.8 Other specified hereditary hemolytic anemias. Stomatocytosis

D58.9 Hereditary hemolytic anemia, unspecified

D59 Acquired hemolytic anemia

D59.0 Drug-induced autoimmune hemolytic anemia.

If it is necessary to identify the drug, use an additional code for external causes (class XX).

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

Cold type (secondary) (symptomatic)

Thermal type (secondary) (symptomatic)

Excludes: Evans syndrome (D69.3)

hemolytic disease of the fetus and newborn (P55. -)

paroxysmal cold hemoglobinuria (D59.6)

D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.

If it is necessary to identify the drug, use an additional code for external causes (class XX).

D59.3 Hemolytic-uremic syndrome

D59.4 Other non-autoimmune hemolytic anemias.

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

D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].

D59.6 Hemoglobinuria due to hemolysis caused by other external causes.

Excludes: hemoglobinuria NOS (R82.3)

D59.8 Other acquired hemolytic anemias

D59.9 Acquired hemolytic anemia, unspecified. Chronic idiopathic hemolytic anemia

D60 Acquired pure red cell aplasia (erythroblastopenia)

Includes: red cell aplasia (acquired) (adults) (with thymoma)

D60.0 Chronic acquired pure red cell aplasia

D60.1 Transient acquired pure red cell aplasia

D60.8 Other acquired pure red cell aplasias

D60.9 Acquired pure red cell aplasia, unspecified

D61 Other aplastic anemias

Excluded: agranulocytosis (D70)

D61.0 Constitutional aplastic anemia.

Aplasia (pure) red cell:

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

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

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

D61.2 Aplastic anemia caused by other external agents.

If it is necessary to identify the cause, use an additional code of external causes (class XX).

D61.3 Idiopathic aplastic anemia

D61.8 Other specified aplastic anemias

D61.9 Aplastic anemia, unspecified. Hypoplastic anemia NOS. Bone marrow hypoplasia. Panmyelophthisis

D62 Acute posthemorrhagic anemia

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

D63 Anemia in chronic diseases classified elsewhere

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

D63.8 Anemia in other chronic diseases classified elsewhere

D64 Other anemias

With excess blasts (D46.2)

With transformation (D46.3)

With sideroblasts (D46.1)

No sideroblasts (D46.0)

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

D64.1 Secondary sideroblastic anemia due to other diseases.

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

D64.2 Secondary sideroblastic anemia caused by drugs or toxins.

If it is necessary to identify the cause, use an additional code of external causes (class XX).

D64.3 Other sideroblastic anemias.

Pyridoxine-reactive, not elsewhere classified

D64.4 Congenital dyserythropoietic anemia. Dyshematopoietic anemia (congenital).

Excludes: Blackfan-Diamond syndrome (D61.0)

DiGuglielmo disease (C94.0)

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

BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS

HEMORRHAGIC CONDITIONS (D65-D69)

D65 Disseminated intravascular coagulation [defibration syndrome]

Afibrinogenemia acquired. Consumptive coagulopathy

Diffuse or disseminated intravascular coagulation

Acquired fibrinolytic bleeding

Excluded: defibration syndrome (complicating):

In a newborn (P60)

D66 Hereditary factor VIII deficiency

Factor VIII deficiency (with functional impairment)

Excludes: factor VIII deficiency with vascular disorder (D68.0)

D67 Hereditary factor IX deficiency

Factor IX (with functional impairment)

Thromboplastic plasma component

D68 Other bleeding disorders

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

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

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

Excludes: hereditary capillary fragility (D69.8)

factor VIII deficiency:

With functional impairment (D66)

D68.1 Hereditary factor XI deficiency. Hemophilia C. Plasma thromboplastin precursor deficiency

D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.

Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease

D68.3 Hemorrhagic disorders caused by anticoagulants circulating in the blood. Hyperheparinemia.

If necessary, identify the anticoagulant used, use an additional external cause code.

D68.4 Acquired coagulation factor deficiency.

Coagulation factor deficiency due to:

Vitamin K deficiency

Excludes: vitamin K deficiency in the newborn (P53)

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

D68.9 Coagulation disorder, unspecified

D69 Purpura and other hemorrhagic conditions

Excludes: benign hypergammaglobulinemic purpura (D89.0)

cryoglobulinemic purpura (D89.1)

idiopathic (hemorrhagic) thrombocythemia (D47.3)

lightning purple (D65)

thrombotic thrombocytopenic purpura (M31.1)

D69.0 Allergic purpura.

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

Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). Thrombocytopathy.

Excludes: von Willebrand disease (D68.0)

D69.2 Other non-thrombocytopenic purpura.

D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome

D69.4 Other primary thrombocytopenias.

Excludes: thrombocytopenia with absent radius (Q87.2)

transient neonatal thrombocytopenia (P61.0)

Wiskott-Aldrich syndrome (D82.0)

D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).

D69.6 Thrombocytopenia, unspecified

D69.8 Other specified hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia

D69.9 Hemorrhagic condition, unspecified

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

D70 Agranulocytosis

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

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

Excludes: transient neonatal neutropenia (P61.5)

D71 Functional disorders of polymorphonuclear neutrophils

Defect of the cell membrane receptor complex. Chronic (children's) granulomatosis. Congenital dysphagocytosis

Progressive septic granulomatosis

D72 Other white blood cell disorders

Excludes: basophilia (D75.8)

immune disorders (D80-D89)

preleukemia (syndrome) (D46.9)

D72.0 Genetic abnormalities of leukocytes.

Anomaly (granulation) (granulocyte) or syndrome:

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

D72.8 Other specified white blood cell disorders.

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

D72.9 White blood cell disorder, unspecified

D73 Diseases of the spleen

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

Excludes: asplenia (congenital) (Q89.0)

D73.2 Chronic congestive splenomegaly

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

Excludes: traumatic splenic rupture (S36.0)

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

D73.9 Disease of the spleen, unspecified

D74 Methemoglobinemia

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

Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia

D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfhemoglobinemia).

Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).

D74.9 Methemoglobinemia, unspecified

D75 Other diseases of the blood and hematopoietic organs

Excludes: swollen lymph nodes (R59. -)

hypergammaglobulinemia NOS (D89.2)

Mesenteric (acute) (chronic) (I88.0)

Excludes: hereditary ovalocytosis (D58.1)

D75.1 Secondary polycythemia.

Decreased plasma volume

D75.2 Essential thrombocytosis.

Excludes: essential (hemorrhagic) thrombocythemia (D47.3)

D75.8 Other specified diseases of the blood and hematopoietic organs. Basophilia

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

D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system

Excludes: Letterer-Sieve disease (C96.0)

malignant histiocytosis (C96.1)

reticuloendotheliosis or reticulosis:

Histiocytic medullary (C96.1)

D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.

Hand-Schueller-Crisgen disease. Histiocytosis X (chronic)

D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.

Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS

D76.2 Hemophagocytic syndrome associated with infection.

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

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

Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma

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

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

SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)

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

caused by human immunodeficiency virus [HIV] sarcoidosis

Excludes: autoimmune diseases (systemic) NOS (M35.9)

functional disorders of polymorphonuclear neutrophils (D71)

human immunodeficiency virus [HIV] disease (B20-B24)

D80 Immunodeficiencies with predominant antibody deficiency

D80.0 Hereditary hypogammaglobulinemia.

Autosomal recessive agammaglobulinemia (Swiss type).

X-linked agammaglobulinemia [Bruton] (with growth hormone deficiency)

D80.1 Non-familial hypogammaglobulinemia. Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS

D80.2 Selective immunoglobulin A deficiency

D80.3 Selective deficiency of immunoglobulin G subclasses

D80.4 Selective immunoglobulin M deficiency

D80.5 Immunodeficiency with increased levels of immunoglobulin M

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

Antibody deficiency with hyperimmunoglobulinemia

D80.7 Transient hypogammaglobulinemia of children

D80.8 Other immunodeficiencies with a predominant antibody defect. Kappa light chain deficiency

D80.9 Immunodeficiency with predominant antibody defect, unspecified

D81 Combined immunodeficiencies

Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)

D81.0 Severe combined immunodeficiency with reticular dysgenesis

D81.1 Severe combined immunodeficiency with low T- and B-cell counts

D81.2 Severe combined immunodeficiency with low or normal B-cell count

D81.3 Adenosine deaminase deficiency

D81.5 Purine nucleoside phosphorylase deficiency

D81.6 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome

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

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

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

D82 Immunodeficiencies associated with other significant defects

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

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

D82.1 Di Georg syndrome. Pharyngeal diverticulum syndrome.

Aplasia or hypoplasia with immune deficiency

D82.2 Immunodeficiency with dwarfism due to short limbs

D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.

X-linked lymphoproliferative disease

D82.4 Hyperimmunoglobulin E syndrome

D82.8 Immunodeficiency associated with other specified significant defects

D82.9 Immunodeficiency associated with significant defect, unspecified

D83 Common variable immunodeficiency

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

D83.1 General variable immunodeficiency with a predominance of disorders of immunoregulatory T cells

D83.2 Common variable immunodeficiency with autoantibodies to B- or T-cells

D83.8 Other common variable immunodeficiencies

D83.9 Common variable immunodeficiency, unspecified

D84 Other immunodeficiencies

D84.0 Lymphocyte functional antigen-1 defect

D84.1 Defect in the complement system. C1 esterase inhibitor deficiency

D84.8 Other specified immunodeficiency disorders

D84.9 Immunodeficiency, unspecified

D86 Sarcoidosis

D86.1 Sarcoidosis of lymph nodes

D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes

D86.8 Sarcoidosis of other specified and combined localizations. Iridocyclitis in sarcoidosis (H22.1).

Multiple cranial nerve palsies in sarcoidosis (G53.2)

Uveoparotitic fever [Herfordt's disease]

D86.9 Sarcoidosis, unspecified

D89 Other disorders involving the immune mechanism, not elsewhere classified

Excludes: hyperglobulinemia NOS (R77.1)

monoclonal gammopathy (D47.2)

non-engraftment and graft rejection (T86. -)

D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS

D89.2 Hypergammaglobulinemia, unspecified

D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified

D89.9 Disorder involving the immune mechanism, unspecified. Immune disease NOS

APLASTIC AND OTHER ANEMIA (D60-D64)

Excluded: refractory anemia:

• NOS (D46.4)
• with excess blasts (D46.2)
• with transformation (C92.0)
• with sideroblasts (D46.1)
• without sideroblasts (D46.0)

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

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

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Posthemorrhagic anemia

Posthemorrhagic anemia is a disease that is accompanied by a decrease in the number of red blood cells and hemoglobin concentration due to massive acute bleeding or as a result of even minor but chronic blood loss.

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

Depending on the root cause and course of posthemorrhagic anemia, acute and chronic forms are distinguished. In accordance with the international classification system, the disease is divided as follows:

• Secondary iron deficiency anemia after blood loss. ICD 10 code D.50
• Acute posthemorrhagic anemia. ICD 10 code D.62.
• Congenital anemia after fetal bleeding – P61.3.

In clinical practice, secondary iron deficiency anemia is also called posthemorrhagic chronic anemia.

Causes of the acute form of the disease

The main reason for the development of acute posthemorrhagic anemia is the loss of a large volume of blood over a short period of time, which occurred as a result of:

• Trauma that caused damage to the main arteries.
• Damage to large blood vessels during surgery.
• Rupture of the fallopian tube during the development of an ectopic pregnancy.
• Diseases of the internal organs (most often the lungs, kidneys, heart, gastrointestinal tract), which can lead to acute massive internal bleeding.

In young children, the causes of acute posthemorrhagic anemia are most often umbilical cord injuries, congenital pathologies of the blood system, damage to the placenta during cesarean section, early placental abruption, placental previa, and birth trauma.

Causes of chronic posthemorrhagic anemia

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

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

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

Symptoms and blood picture of anemia due to acute blood loss

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

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

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

Here you will find detailed information about treatment methods

Anemia-Symptoms and Treatment https://youtu.be/f5HXbNbBf5w Iron deficiency

This video takes a closer look at normal

About Chapter 19.08.

About Chapter 19.08.

Dr. Komarovsky will explain what causes an

Subscribe to the channel "About the most important" ▻ https://www.y

Instagram: https://www.instagram.com/dr.philipp VK: https://vk.com/doctorphil What is it?

Subscribe to the channel "About the most important" ▻ https://www.y

Subscribe to the channel "About the most important" ▻ https://www.y

Anemia is a condition that occurs in almost all

Hemolytic anemia is anemia that develops in the

In this video, Oleg Gennadievich Torsunov talks about the

http://svetlyua.ru/Anemia, treatment with folk remedieshttp://sve

Good afternoon dear friends! Dietitian-nutritionist with you

I'm on: INSTAGRAM http://instagram.com/julia__rain TWITTER https://twitter.com/JuliaRain4 VKONTAKT

Anemia or anemia is a decrease in the concentration of g�

How to treat anemia? What helped me with iron deficiency?

Iron-deficiency anemia. Symptoms, Signs and Methods�

Anemia is one of the most common causes of prolapse

Changes in blood test results within a few days after bleeding has stopped and the development of anemia are closely related to compensation mechanisms that “turn on” in the body in response to the loss of a large volume of blood. They can be divided into the following stages:

• The reflex phase, which develops on the first day after blood loss. Redistribution and centralization of blood circulation begins, peripheral vascular resistance increases. In this case, a decrease in the number of red blood cells is observed at normal values ​​​​of hemoglobin concentration and hematocrit.
• The hydremic phase occurs from the second to the fourth day. Extracellular fluid enters the vessels, glycogenolysis is activated in the liver, which leads to an increase in glucose content. Gradually, symptoms of anemia appear in the blood picture: the concentration of hemoglobin decreases, the hematocrit decreases. However, the color index value is still normal. Due to the activation of thrombus formation processes, the number of platelets decreases, and due to the loss of leukocytes during bleeding, leukopenia is observed.
• The bone marrow phase begins on the fifth day after bleeding. Insufficient oxygen supply to organs and tissues activates hematopoietic processes. In addition to decreased hemoglobin, hematocrit, thrombocytopenia and leukopenia, at this stage there is a decrease in the total number of red blood cells. When examining a blood smear, the presence of young forms of red blood cells is noted: reticulocytes, sometimes erythroblasts.

Similar changes in the blood picture are described in many situational tasks for future doctors.

Symptoms and diagnosis of anemia in chronic bleeding

Chronic posthemorrhagic anemia is similar in its symptoms to iron deficiency, since regular, mild bleeding leads to a deficiency of this microelement. The course of this blood disease depends on its severity. It is determined depending on the concentration of hemoglobin. Normally, in men it is 135–160 g/l, and in women 120–140 g/l. In children, this value varies depending on age from 200 in infants to 150 in adolescents.

Degree of posthemorrhagic chronic anemia Hemoglobin concentration

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

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

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

A severe degree of anemia is manifested by numbness and a tingling feeling in the fingers and toes, specific taste preferences appear, for example, some patients begin to eat chalk, and the perception of smells changes. Very often this stage of chronic posthemorrhagic anemia is accompanied by rapidly progressing caries and stomatitis.

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

Treatment of anemia after massive blood loss

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

After identifying the source and stopping the bleeding, it is urgently necessary to restore the blood supply to the vessels. For this purpose, rheopolyglucin, hemodez, polyglucin are prescribed. Acute blood loss is also compensated by blood transfusion, taking into account the compatibility of the Rh factor and blood group. The volume of blood transfusion is usually 400 – 500 ml. These measures must be carried out very quickly, since a rapid loss of even ¼ of the total blood volume can be fatal.

After stopping the state of shock and carrying out all the necessary manipulations, they proceed to standard treatment, which consists of the administration of iron supplements and enhanced nutrition to compensate for the deficiency of vitamins and microelements. Ferrum lek, ferlatum, maltofer are usually prescribed.

Typically, restoration of a normal blood picture occurs after 6–8 weeks, but the use of medications to normalize hematopoiesis continues for up to six months.

Treatment of chronic posthemorrhagic anemia

The first and most important step in the treatment of posthemorrhagic chronic anemia is to determine the source of bleeding and its elimination. Even the loss of 10 - 15 ml of blood per day deprives the body of the entire amount of iron that was received during that day with food.

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

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

In severe cases of posthemorrhagic chronic anemia, red blood cell transfusion and injection of drugs with iron are indicated to stimulate hematopoietic processes. Ferlatum, maltofer, likferr and similar medications are prescribed.

Recovery after the main course of treatment

The duration of taking iron-containing drugs is determined by the doctor. In addition to the use of various medications to restore normal oxygen supply to organs and replenish iron reserves in the body, proper nutrition is very important.

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

When creating a diet, attention should be paid not only to how much iron a particular product contains, but also to the degree of its absorption in the body. It increases with the consumption of vegetables and fruits that contain vitamins B and C. These are citrus fruits, black currants, raspberries, etc.

Course and treatment of posthemorrhagic anemia in children

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

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

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

With timely initiation of treatment and non-critical blood loss, the prognosis is generally favorable. After compensation for iron deficiency, the child quickly recovers.

As is already known, posthemorrhagic anemia occurs in the human body due to blood loss. Moreover, it will not necessarily be abundant. It is important to understand that even minor bleeding, but occurring frequently, can become seriously dangerous for the patient.

Posthemorrhagic anemia: code according to ICD-10

Distribution of diseases according to this classification (regarding the acute course of the disease) – D62. This classification also indicates that the cause of the disease is considered to be blood loss of any nature.

Posthemorrhagic anemia: severity levels

The severity of this type of anemia also depends on the hemoglobin level. The first degree of severity is characterized by a hemoglobin content in the blood of more than 100 grams per liter of blood and red blood cells above 3 t/l. If the hemoglobin level in the blood reaches 66 - 100 g/l and the number of red blood cells is above 2 - 3 t/l, we can talk about the occurrence of moderate severity of posthemorrhagic anemia. Finally, we are talking about a severe stage of anemia if hemoglobin drops below 66 g/l.

If a mild degree of severity of this type of anemia is detected in time, the patient can still be helped. In this case, the main goal of treatment is to replenish iron reserves in the body. Taking appropriate iron supplements can help with this. Only a doctor can prescribe such drugs in accordance with the patient’s tests and his individual complaints. It is important that the preparation contains a component that promotes the complete absorption of iron. This component may be, for example, ascorbic acid. Sometimes hospital treatment may be required.

For posthemorrhagic anemia of moderate severity, posthemorrhagic anemia requires taking appropriate medications. As for the severe degree, hospitalization of the patient is urgently indicated. Delay in this case could cost the patient his life.

Posthemorrhagic anemia: causes of the disease

A lack of blood in the body can be caused by:

1. Violation of normal hemostasis. Hemostasis is designed to keep the blood in a liquid state, that is, as it should be normally. It is also responsible for normal blood clotting;
2. Lung diseases. Such diseases can be judged by scarlet bleeding in the form of liquid or clots that occurs when coughing;
3. Trauma due to which vascular integrity was compromised, mainly affecting large arteries;
4. Ectopic pregnancy. With this problem, severe internal bleeding is observed, which causes the development of acute posthemorrhagic anemia;
5. Surgical intervention. Almost any operation involves blood loss. It is not always abundant, but this may be enough for the development of pathology;
6. Stomach and duodenal ulcers. Internal bleeding is common with such diseases. Such bleeding cannot always be quickly recognized. But if this is not done on time, death is possible.

Posthemorrhagic anemia: stages

There are two stages of this pathology – acute and chronic. Acute begins due to rapid and massive blood loss. Such blood loss is often caused by injury, internal and external bleeding, and surgical intervention during which blood vessels are injured. The chronic stage of the disease is characterized by moderate bleeding, which occurs quite often, for example, we are talking about hemorrhoids and peptic ulcers. The same applies to girls with menstrual cycle abnormalities and uterine fibromatosis. The same goes for nosebleeds.

Pathogenesis of posthemorrhagic anemia

The key factors of this type of anemia are the phenomena of vascular insufficiency. At the same time, blood pressure decreases, blood supply to tissues and internal organs is disrupted, hypoxia and ischemia are observed, and a state of shock may become possible.

The first phase is called early reflex-vascular. It is also called hidden anemia. At the same time, hemoglobin and red blood cell levels are still close to normal. The second phase is the hydremic phase of compensation. It is characterized by the entry of tissue fluid into the bloodstream and the normalization of plasma volume. The decrease in the number of red blood cells begins quite sharply. In the third phase, there is a strong decrease in the amount of formed elements in the blood and the situation begins to get out of control.

Acute posthemorrhagic anemia: ICD-10

What can be said about the stages of this type of anemia? Chronic posthemorrhagic anemia is something that is difficult to combat, since the causes lie in some other disorders in the body. That is why we will talk about acute posthemorrhagic anemia.

With acute blood loss, by which we mean more than 1000 ml of blood, in a short period of time, the patient may experience collapse and shock.

Acute anemia: causes (post-hemorrhagic) - what are they? They are most often associated with unforeseen injuries.

If we talk about the symptoms of acute hemorrhagic anemia, they are represented by gastrointestinal disorders, dizziness, and nausea. In addition, the patient may feel weak, his skin may become pale and his blood pressure may drop.

Treatment of posthemorrhagic anemia

Therapy for this disease is carried out only in a hospital setting. The fact is that bleeding, especially massive bleeding under other conditions, cannot always be stopped. Sometimes infusion-transfusion therapy and surgical intervention are needed.

After bleeding has stopped, you should start taking iron supplements, and only at the discretion of your doctor. In the severe stage, it will be necessary to administer drugs intravenously; in the mild stage, taking tablets orally is sufficient. In some cases, combined treatment with both methods is indicated.

Posthemorrhagic anemia is a set of pathological changes that develop in the body due to the loss of a certain amount of blood: it contains iron, and with blood loss it becomes insufficient. It is divided into two types: acute and chronic.

ICD-10 code

Chronic posthemorrhagic anemia has the following ICD-10 code - D50.0, and acute - D62. These disorders are located in the section “Anemia associated with nutrition. Iron-deficiency anemia".

Latin defines the word anemia as “lack of blood,” literally speaking. The word can also be translated as “anemia,” which means a lack of hemoglobin. And “hemorrhagic” is translated as “accompanied by bleeding,” the prefix “post” means “after.”

Information about what posthemorrhagic anemia is will allow you to detect its development in time and provide the necessary assistance.

Pathogenesis in posthemorrhagic anemia

Pathogenesis is a certain sequence of development of pathological changes, which makes it possible to judge the features of the occurrence of posthemorrhagic anemia.

The severity of posthemorrhagic anemia is determined by the hemoglobin content and the severity of tissue hypoxia due to its deficiency, but the symptoms of anemia and its features are associated not only with this indicator, but also with others that decrease with blood loss:

• Iron content;
• Potassium;
• Magnesium;
• Copper.

Iron deficiency has a particularly negative effect on the circulatory system, in which the production of new blood elements is difficult.

The minimum volume of blood that can be lost without the risk of developing serious disorders is 500 ml.

Donors donate blood without exceeding this amount. A healthy human body with sufficient body weight completely restores lost elements over time.

When there is not enough blood, small vessels constrict to compensate for the shortage and maintain blood pressure at a normal level.

Due to a lack of venous blood, the heart muscle begins to work more actively to maintain sufficient minute blood flow - the amount of blood that is ejected by the heart per minute.

What color of venous blood can you read?

Read what the heart muscle consists of

The functioning of the heart muscle is impaired due to mineral deficiency, the heart rate decreases, and the pulse weakens.

An arteriovenous shunt (fistula) occurs between the veins and arterioles, and blood flows through the anastomoses without touching the capillaries, which leads to impaired blood circulation in the skin, muscular system, and tissues.

Formation of an arteriovenous shunt, due to which blood does not flow to the capillaries

This system exists to maintain blood flow to the brain and heart, allowing them to continue to function even in the face of severe blood loss.

Interstitial fluid quickly compensates for the lack of plasma (the liquid part of the blood), but microcirculation disturbances persist. If blood pressure drops significantly, the speed of blood flow in small vessels will decrease, leading to thrombosis.

In the severe stage of posthemorrhagic anemia, small blood clots form that clog small vessels, which leads to disruption of the functioning of the arterial glomeruli in the kidney tissue: they do not filter fluid properly, and the amount of urine excreted is reduced, and harmful substances are retained in the body.

Blood circulation in the liver also weakens. If acute posthemorrhagic anemia is not treated promptly, it will lead to liver failure.

With posthemorrhagic anemia, the liver suffers due to lack of blood

Oxygen deficiency in tissues leads to the accumulation of under-oxidized elements that poison the brain.

Acidosis develops: a violation of the acid-base balance towards the predominance of an acidic environment. If posthemorrhagic anemia is severe, the amount of alkalis is reduced, and the symptoms of acidosis increase.

With blood loss, the level of platelets decreases, but this has little effect on the coagulation processes: the content of other substances that affect coagulation reflexively increases.

Over time, the clotting mechanisms return to normal, but there is a risk of developing thrombohemorrhagic syndrome.

Causes

The main factor influencing the development of posthemorrhagic anemia is blood loss, the causes of which can be different.

Acute posthemorrhagic anemia

This is a disorder that develops rapidly due to excessive blood loss. This is a dangerous condition that requires rapid initiation of treatment measures.

Causes of acute anemia:

Chronic posthemorrhagic anemia

A condition that develops with systematic blood loss over a long period of time. It can go unnoticed for a long time if the blood loss is mild.

Causes of chronic anemia:

Hemorrhagic anemia also develops due to vitamin C deficiency.

Kinds

Posthemorrhagic anemia is divided not only by the nature of its course (acute or chronic), but also by other criteria.

The severity of anemia is assessed by the amount of hemoglobin in the blood.

Depending on its content, anemia is divided into:

• Light. With mild anemia, hemoglobin begins to lack iron, its production is impaired, but the symptoms of anemia are practically absent. Hemoglobin does not fall below 90 g/l.
• Average. Symptoms with moderate severity are moderate, hemoglobin concentration is 70-90 g/l.
• Heavy. In severe cases, serious organ dysfunction is observed, heart failure develops, and the structure of hair, teeth, and nails changes. Hemoglobin content is 50-70 g/l.
• Extremely severe. If the hemoglobin level is below 50 g/l, there is a risk of life.

There are also certain pathologies included in the ICD:

• Congenital anemia in the newborn and fetus due to blood loss (code P61.3);
• Posthemorrhagic anemia of the chronic type, which is secondary iron deficiency (code D50.0).

Symptoms

Acute form of anemia

Symptoms in the acute form of posthemorrhagic anemia increase very quickly and depend on the severity of blood loss.

Observed:

A decrease in blood pressure due to massive blood loss is called hemorrhagic shock. The intensity of the fall in blood pressure depends on the severity of blood loss.

The following symptoms are also present:

• Tachycardia;
• The skin is cold and pale, with moderate and severe degrees it has a cyanotic (bluish) color;
• Impaired consciousness (stupor, coma, loss of consciousness);
• Weak pulse (if the stage is severe, it can only be felt on the main vessels);
• Reducing the amount of urine excreted.

The symptoms of posthemorrhagic anemia and hemorrhagic shock are joined by signs that are inherent to the disease that caused blood loss:

• With an ulcer, black or red stool is observed;
• Swelling in the impact area (if injured);
• When the arteries in the lungs rupture, there is a cough with bright scarlet blood;
• Intense bloody discharge from the genitals during uterine bleeding.

The source of bleeding is identified by indirect signs depending on the clinical picture.

Stages of acute posthemorrhagic syndrome

Acute posthemorrhagic syndrome has three stages of development.

Name	Description
Reflex-vascular stage	The level of plasma and red blood cells drops, compensatory processes are activated, blood pressure drops, and the heart rate increases.
Hydremia stage	It develops several hours after blood loss and lasts from 2 to 3 days. Intercellular fluid restores the volume of fluid in the vessels. The content of red blood cells and hemoglobin decreases.
Bone marrow stage	Develops 4-5 days after blood loss due to oxygen starvation. The level of hematopoietin and reticulocytes, the precursor cells of red blood cells, increases in the blood. The amount of iron in the plasma decreases.

The body fully recovers after blood loss after two to three or more months.

Signs of chronic form

Chronic bleeding gradually leads to posthemorrhagic anemia, which develops gradually, and its symptoms are closely related to the severity of hemoglobin deficiency.

Observed:

People with posthemorrhagic anemia have low immunity and often develop infectious diseases.

Diagnostics

In case of acute blood loss, the patient remains in hospital treatment so that risks can be assessed and timely assistance provided.

Laboratory diagnosis of posthemorrhagic anemia is carried out repeatedly, and the results vary depending on the stage and severity of the disorder.

Laboratory signs of acute anemia:

• In the first two hours, the concentration of platelets increases, and red blood cells and hemoglobin remain at normal levels;
• After 2-4 hours, the excess platelets remain, neutrophil granulocytes grow in the blood, the concentration of red blood cells and hemoglobin decreases, according to the color indicator, anemia is defined as normochromic (normal value);
• After 5 days, an increase in reticulocytes is noted, the iron level is insufficient.

What tests need to be taken?

It is necessary to take a general blood test; in case of chronic anemia, it reveals the content of elliptocytes; lymphocytes are increased in the peripheral blood, but reduced in the overall cellular composition.

A deficiency of iron, calcium, and copper is detected. Increased manganese content.

In parallel, tests are carried out to determine the cause of bleeding: stool examination for helminthiasis and occult blood, colonoscopy, urinalysis, bone marrow examination, ultrasound examination, esophagogastroduodenoscopy, electrocardiogram.

Who to contact?

Hematologist

Treatment

Acute hemorrhagic anemia at the first stage of treatment requires eliminating the cause of blood loss and restoring normal blood volume.

Surgeries are performed to suture wounds and blood vessels, and the following medications are prescribed:

• Artificial blood substitutes. They are infused by drop or stream, depending on the patient’s condition;
• When shock develops, the use of steroids (Prednisolone) is indicated;
• Soda solution eliminates acidosis;
• Anticoagulants are used to eliminate blood clots in small vessels.
• If blood loss exceeds a liter, a donor blood transfusion is necessary.

Treatment of chronic anemia not complicated by serious diseases is carried out on an outpatient basis. Nutrition correction with the addition of foods containing iron, vitamins B9, B12 and C is indicated.

In parallel, treatment is carried out for the underlying disease that caused the pathological changes.

Forecast

If, after extensive blood loss, the patient quickly arrived at the hospital and received the full range of treatment procedures aimed at restoring blood levels and eliminating bleeding, then the prognosis is favorable, except in cases where the blood loss is extremely severe.

A chronic type of pathology is successfully eliminated by curing the disease that caused it. The prognosis depends on the severity of concomitant diseases and the degree of neglect of anemia. The sooner the cause is identified and treatment is started, the greater the chances of a favorable outcome.

Video: Anemia. How to treat anemia?

Posthemorrhagic anemia is a lack of iron-containing elements in human blood plasma. Anemia resulting from blood loss is one of the most common anemias. Doctors distinguish two forms of this disease: chronic and acute.

Posthemorrhagic anemia of a chronic nature occurs after small but, for some time, frequent bleeding. The acute form of this disease occurs due to sudden, heavy blood loss.

The minimum volume of blood loss in an adult that is dangerous to human life is 500 ml.

According to the International Classification of Diseases, 10th revision, posthemorrhagic anemia belongs to the category “Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism.” Subsection: "Anemia associated with nutrition. Iron deficiency anemia." The classification of diseases with codes is as follows:

• Iron deficiency anemia secondary to blood loss (chronic) – code D50.0.
• Acute posthemorrhagic anemia - code D62.
• Congenital anemia due to fetal blood loss - code P61.3

, , , , , , ,

ICD-10 code

D62 Acute posthemorrhagic anemia

D50.0 Iron deficiency anemia secondary to blood loss, chronic

Causes of posthemorrhagic anemia

The etiology of a lack of blood in the body can be:

• Trauma resulting in a violation of the integrity of blood vessels, especially large arteries.
• Surgical intervention. Any surgical intervention is always a risk. When starting even the simplest operation for a seemingly ordinary person, the surgeon is not able to foresee all its nuances and consequences.
• Ulcer of the duodenum and stomach. These diseases are often accompanied by internal bleeding. And the difficulty of their timely detection is that the bleeding occurs inside the body and externally it can be recognized by an amateur by certain signs and an ambulance can be called in time. Otherwise, delay may result in death for the patient.
• Impaired hemostasis. This factor is designed to maintain blood in a liquid state, being responsible for the blood clotting rate, which makes it possible to maintain circulating blood volumes within normal limits and normalize the composition (“formula”) of blood.
• Ectopic pregnancy. This pathology is accompanied in women by acute heavy bleeding, which leads to acute posthemorrhagic anemia.
• Pulmonary diseases. This bleeding is manifested by scarlet discharge with a liquid or clot-like consistency that occurs during coughing.

Pathogenesis

Pathogenesis, or the sequence of occurring phenomena, constitutes the phenomena of vascular insufficiency, due to a sudden emptying of blood (plasma) from the vascular bed. These factors lead to a lack of red blood cells that carry oxygen, which, in turn, leads to general oxygen starvation of the body. The body will not be able to compensate for this loss on its own due to the more active work of the heart.

, , , , ,

Symptoms of posthemorrhagic anemia

Knowledge won't hurt anyone. And in order to be able to recognize bleeding (especially if it is internal), it is necessary to know the symptoms of posthemorrhagic anemia and its manifestations in order to provide first aid or call an ambulance in time.

• With heavy blood loss, vascular manifestations come first: shortness of breath, rapid heartbeat (tachycardia), and decreased blood pressure (both arterial and venous).
• The patient's skin and mucous membranes become pale.
• The patient begins to feel darkening in the eyes, tinnitus and slight dizziness.
• A gag reflex may appear.
• An acute sign of internal bleeding can be considered severe dry mouth. The severity of the clinic is determined not only by the total volume of sweat, but also by the rate at which the victim loses blood.
• The location of the injury is also an important factor. Thus, damage to the gastrointestinal tract is accompanied by a sharp increase in body temperature.
• Obvious manifestations of intoxication.
• The level of residual nitrogen in the plasma also increases its performance (while the urea level remains normal).
• Even with small amounts of internal bleeding, the patient feels compression of the organs.
• Fecal discharge can also be an indicator of internal damage. Due to the excreted blood, they turn black.

Acute posthemorrhagic anemia

If a person loses, as a result of injury (the consequence of which is damage to a large artery), an operation being performed or an exacerbation of any disease, an eighth of the total volume of working blood, an acute form of posthemorrhagic anemia occurs.

Doctors distinguish several stages of development of acute anemia:

1. Reflex-vascular stage. It is expressed by a sharp decrease in blood pressure, pallor of the skin and mucous membranes, and tachycardia. A sudden lack of oxygen reaching the organs leads to spasms of peripheral blood vessels. To prevent a further drop in pressure, the body opens arteriole-venular shunts, leading to the removal of plasma from the organs. This therapy itself works to adequately compensate the return of blood fluid to the heart.
2. Hydremic stage. After three to five hours, the basis for hydremic compensation is created, caused by the flow of fluid from the interstitial area into the blood vessels. In this case, certain receptors are irritated, which are involved in maintaining the volume of fluid circulating through the vessels. Increased synthesis of aldosterone blocks the removal of sodium from the body, which stimulates water retention. However, this also leads to plasma dilution, and as a consequence, a decrease in the content of red blood cells and hemoglobin. This stage of compensation can take place within two to three days.
3. Bone marrow stage - this stage occurs four to five days from the moment of bleeding. Hypoxia progresses. Erythropoietin levels are increasing. In the peripheral blood, the number of newly formed red blood cells (reticulocytes), which have a reduced amount of hemoglobin, increases. The characteristic of this stage becomes hypochromic. In addition, a sharp lack of blood causes a decrease in iron in the blood.

Chronic posthemorrhagic anemia

This type of anemia, chronic posthemorrhagic anemia, occurs in a patient if he gradually, over a period of time, loses blood in fractions. This type of anemia can occur in a number of diseases. For example, such as: intestinal cancer, peptic ulcer of the duodenum or stomach, gingivitis, hemorrhoids, and many others. Frequent but minor bleeding leads to general exhaustion of the body. Iron deficiency occurs. In this regard, this pathology, according to its etiology, is classified as posthemorrhagic anemia; according to its pathogenesis, this pathological condition can be classified as iron deficiency anemia.

Based on this, the main goal of therapy for posthemorrhagic anemia, in any of its forms, is to restore the full volume of blood plasma circulating in the vessels, and, as a consequence, to overcome iron deficiency and lack of erythropoiesis. But this is an “ambulance” for the body. After emergency resuscitation, it is necessary to turn your attention to the root cause that caused the bleeding. And it’s simpler - you need to start treating the underlying disease.

, , , , ,

Posthemorrhagic iron deficiency anemia

Today, doctors note that posthemorrhagic iron deficiency anemia is beginning to become quite widespread. In short, iron deficiency anemia is a condition of the body characterized by a pathological lack of iron ions. Moreover, the mass concentration of this element decreases everywhere: in the blood plasma, in the bone marrow, and in the so-called storage room, where the body accumulates everything it needs in reserve. As a result, a failure occurs in the heme synthesis system, resulting in a deficiency of myoglobin and tissue enzyme.

Modern statistical studies voice a figure of 50% - this is the amount of the population that suffers from anemia in one form or another. Compounds in which metals occur in nature are poorly absorbed or not absorbed at all by the human body. When the balance in the intake of iron into the body and its use is disturbed, we get iron deficiency anemia.

Most often, in the adult population, iron deficiency is associated with acute or chronic blood loss. This diagnosis can occur, although quite rarely, with nosebleeds, dental aspects of blood loss, as well as with trauma... Exceptional cases have also been identified when iron deficiency anemia developed in a donor who “frequently gave blood.” Moreover, strange as it may sound, such deviations are found in female donors.

In women, the causes of the disease can be both uterine bleeding and pregnancy itself, as well as painful, pathological disruptions in the menstrual cycle. Laboratory studies show that uterine fibroids can also lead to posthemorrhagic anemia with iron deficiency, which contributes to the leaching of iron and the subsequent appearance of anemic symptoms.

The second place in the frequency of diseases is occupied by blood loss in acute diseases of the gastrointestinal tract, which are quite problematic to diagnose in the early stages. Pulmonary hemorrhage is a fairly rare manifestation of iron deficiency, as is blood loss from the urinary tract and kidneys.

Newborns and infants may suffer from iron deficiency due to abnormal placenta previa or if it is damaged during surgery (cesarean section). There are also cases of intestinal bleeding as a manifestation of an infectious disease.

The reason for the lack of iron in older children may also be a poor diet. The baby simply does not receive enough of the element from the foods he eats. Anemia can also be caused by a lack of iron in the mother during her pregnancy, as well as in premature babies or babies of twins and triplets... Quite rarely, but the cause of this disease can also be the mistake of the obstetrician, who, without waiting for the pulsation to stop, cut the umbilical cord early.

You should not ignore the situation when (for example, during heavy physical activity, pregnancy, etc.) the body’s need for it sharply increases. Therefore, the likelihood of posthemorrhagic iron deficiency anemia increases.

The lack of this element in the body causes significant harm to the human immune system. But, strange as it may sound, patients suffering from iron deficiency suffer less from infectious diseases. It's simple. Iron is an excellent nutrient medium for some bacteria. However, in light of other problems, iron deficiency in the human body cannot be ignored. There are often cases when a lack of iron in the blood is indicated by changed eating habits. For example, a previously unobserved craving for peppery or salty foods appears.

Doctors also highlight the psychological aspect of iron deficiency. It often occurs in people who do not care about their health, and, consequently, about themselves: diets, limited nutrition, physical inactivity, lack of fresh air, a minimum of positive emotions. All this does not contribute, but rather inhibits the metabolic processes that occur in the body. After conducting a study, scientists found that behind all this, as a rule, there is deep depression and psychological trauma.

Today, medicine is equipped with a fairly large arsenal in the form of iron preparations: conferon, feramide, jectofer, sorbifer and quite a lot of others. There are also liquid forms, for example, maltofer, the degree of absorption of which depends on the level of iron deficiency in the body. This drug is approved for use even for newborns (even premature babies).

Posthemorrhagic anemia in children

Posthemorrhagic anemia in children occurs quite often and, like in adults, can be acute (quite common) or chronic (less common).

Newborns are quite vulnerable. In them, posthemorrhagic anemia quite often occurs due to birth injuries or can even occur with excessive blood sampling during laboratory tests. In older and middle-aged children, the main cause of anemia is often helminths, which, by sticking to the wall of the gastrointestinal tract, injure the body and provoke microbleeding.

Symptoms for which parents should raise the alarm:

• The same as for adults.
• But the first manifestations are lethargy, loss of appetite, growth cessation occurs, and the baby begins to gain weight worse.
• One of the primary signs of the initial stage of the disease may be a change in the baby’s taste preferences, to the point that children tend to eat soil, chalk, clay... This is the result of iron deficiency and lack of mineral components in the baby’s body. Sometimes these changes are not so radical.
• There is also a change in behavior. Kids become capricious and whiny, or, in contrast, apathetic.
• There are also external manifestations: brittle hair and nails, peeling skin.
• “Vacquered” smooth tongue.
• In teenage girls, interruptions in the menstrual cycle.
• Quite often, against the background of posthemorrhagic anemia, complications of an infectious nature are observed: otitis media, pneumonia...

The first thing that needs to be done in a situation where a child is in a state of hemorrhagic shock is resuscitation measures to stop bleeding and anti-shock therapy. Blood substitutes are administered by stream and drip. During this period, the baby’s blood type and Rhesus status are determined. Resuscitation is carried out with freshly citrated blood. If one is not available, a direct transfusion from the donor is performed. In parallel with this, glycosides support the cardiovascular system and a diet rich in protein and vitamins is prescribed.

Treatment of posthemorrhagic anemia in children involves identifying and treating the root cause of bleeding, that is, the disease that caused blood loss.

Stages

Doctors also have a so-called working classification of the stages of anemia severity, which is determined on the basis of laboratory tests:

• when the hemoglobin content in the blood is more than 100 g/l and erythrocytes are above 3 t/l - a mild stage.
• when the hemoglobin content in the blood is within 100÷66 g/l and erythrocytes above 3÷2 t/l - the middle stage.
• when the hemoglobin content in the blood is less than 66 g/l – a severe stage.

Mild posthemorrhagic anemia

Earlier detection of the disease allows the child to get back on his feet in a shorter period of time. At a mild stage of the disease, sometimes iron-containing drugs are enough to replenish the lack of iron in the body. The course of treatment often lasts three months or more. In this case, temporary hospitalization of the patient is possible. This issue is decided by the doctor based on the patient’s condition.

Severe posthemorrhagic anemia

Severe posthemorrhagic anemia is an unconditional hospitalization.

Only in a hospital setting can a patient receive qualified and full medical care, and there is no point in delaying this. In this situation, “delay is like death.”

Having received the patient at their disposal, doctors, first of all, must do everything to stop the bleeding, while at the same time trying to compensate for blood loss by any means. To obtain the maximum hemodynamic effect (removing the patient from a state of shock, obtaining higher blood pressure, etc.), a transfusion of at least half a liter of polyglucin (an artificial plasma substitute) is performed. In the acute traumatic form, this drug is administered initially as a bolus, and the doctor is required to monitor the blood pressure. If the pressure was brought to the following values: systolic - 100÷110 mm, diastolic - 50÷60 mm, the dropper is switched from jet to drip feed. The total dose of the administered solution can reach, if necessary, one and a half liters (maximum 2÷3 l).

Only after stopping the bleeding and removing the main shock symptoms, the medical staff proceeds to a further, planned protocol for removing the patient from the anemic state.

Diagnosis of posthemorrhagic anemia

Modern medicine cannot be imagined without laboratories and modern medical equipment. But without highly professional specialists, no equipment will help. And in the case of diagnosing posthemorrhagic anemia, the situation is as follows: the diagnosis of acute or chronic posthemorrhagic anemia can be made based on a combination of clinical, laboratory and anamnestic data. Basic are clinical indicators.

Having an external source of bleeding, it is not difficult to make a clear diagnosis; it is more difficult to diagnose it with internal blood loss. The main thing is to accurately determine the location of the outflow.

, , , , , , , ,

Blood test for posthemorrhagic anemia

The first thing doctors need to do is urgently do a detailed blood test so that they can assess the level of blood loss and, accordingly, the danger to the patient. During the first half hour of acute blood loss, the number of platelets increases sharply, which leads to a reduction in the period of time during which blood clotting occurs, which is quite important in case of blood loss. The level of red blood cells and hemoglobin in plasma remains within normal limits for some time, although their total number (red blood cells) decreases.

After two to three hours, thrombocytosis in the blood is still observed, but tests show the appearance of neutrophilic leukocytosis. A high level of thrombocytosis and a short period during which the blood clots are a criterion indicating heavy blood loss. Next comes a decrease in the number of red blood cells and hemoglobin. This is an indicator of the development of normochromic posthemorrhagic anemia.

After five to six days from the critical moment, the number of reticulocytes increases (the formation of young leukocytes). If no repeated bleeding is observed during this period, then after a couple of weeks, the composition of the peripheral blood returns to normal, as tests show. If posthemorrhagic anemia was observed in severe form, then the recovery period will be longer.

Even in the case of a single acute bleeding, biochemical analysis shows a sharp drop in plasma iron levels. With small reserves of this element in the body itself, its quantitative restoration is quite slow. During this period, the active appearance of new red blood cells in the red bone marrow is also visible.

Clinical analysis during the illness shows the presence of leukopenia with slight lymphocytosis. Due to low iron levels, there is an increase in the ability to bind serum iron.

, , , , ,

Treatment of posthemorrhagic anemia

If a mild form of posthemorrhagic anemia can be treated at home, then its acute manifestations must be stopped only in a hospital setting. The main goal of all measures taken is to stop blood loss and restore normal, full blood circulation.

The first stage of treatment is to stop the bleeding. A drop in hemoglobin level to 80 g/l and below (8 g), plasma hematocrit - below 25%, and protein - less than 50 g/l (5 g%) is an indication for transfusion therapy. During this period, it is necessary to replenish the content of red blood cells by at least a third. There is an urgent need to replenish normal plasma volume. In this regard, the patient receives colloidal solutions of polyglucin or gelatinol by transfusion. If such solutions are not available, they can be replaced with 1000 ml of glucose (10%), and then 500 ml of a 5% solution. Reopolyglucin (and analogues) are not used in this situation, as they reduce blood clotting ability, which can provoke re-bleeding.

To restore the level of red blood cells, the patient receives packed red blood cells. In case of acute blood loss, when the platelet count also drops, doctors resort to direct transfusion or transfusion of blood immediately taken before the procedure.

Today, if blood loss during surgery is less than 1 liter, packed red blood cells and transfusion are not used. Full compensation of blood loss is not carried out, since the danger lies in the possibility of disseminated intravascular coagulation syndrome, as well as immune conflict.

Divalent iron is most often used in medicine. Medicines based on it are taken by the patient as prescribed by the doctor either 1 hour before eating or 2 hours after eating. In the treatment of posthemorrhagic anemia, the following iron-containing drugs are used:

• Feramide is a drug based on a compound of nicotinamide and ferric chloride. The dose is taken three times a day, 3÷4 tablets. The disadvantage of this drug is the low iron content in the tablet. To get the maximum effect, you need to take ascorbic acid along with the medicine.
• Conferon – complex content of sodium dioctyl sulfosuccinate with iron sulfate. Release form: capsules. This drug is well absorbed by the intestinal mucosa. Take it 3 times a day, 1÷2 capsules. Additional intake of ascorbic acid is not required.
• Ferrocal. Composition - iron sulfate with calcium fructose diphosphate. Prescribed after meals, 1÷2 tablets three times a day.
• Ferroplex is a combination of ferrous sulfate and ascorbic acid. The dose is 2÷3 tablets three times a day. The tolerability and absorption properties of the drug are excellent.
• Ferroceron. The basis of the drug is the sodium salt of ortho-carboxybenzoylferrocene. The medicine is well absorbed by the gastrointestinal mucosa. Take 1÷2 tablets three times a day. Easy to carry. Hydrochloric and ascorbic acids should not be introduced into the body along with this medicine. It is absolutely necessary to remove lemons and other acidic foods from food.

Other drugs are also used.

Nutrition plays an important role in the treatment of posthemorrhagic anemia. A patient with anemia should include in his diet foods containing large amounts of iron and protein substances. This includes meat, egg whites, fish, cottage cheese... At the same time, remove fatty foods from your diet.

Prevention

Prevention of posthemorrhagic anemia must begin, no less, in the womb. If the mother of the unborn child suffers from iron deficiency, the newborn will be born already having the same problem. Therefore, it is necessary to first eliminate this problem in a pregnant woman. Then, the already born child should receive natural, rational and natural feeding. It is necessary that the baby is surrounded by a normal healthy environment. Constant monitoring by a pediatrician is also needed so as not to miss the development of rickets, infectious diseases and dystrophy.

A special risk group for iron deficiency includes children born from an anemic mother, premature babies and babies from multiple pregnancies, as well as infants receiving artificial, irrational feeding and growing rapidly. For such children, the pediatrician usually prescribes iron supplements or infant formula containing a higher percentage of this element.

For children in the first year of life, as a preventive measure for posthemorrhagic anemia, it is necessary to include vegetables and fruits, cereals and herbs, meat and fish, milk and cheeses in their diet. That is, diversify your diet. To maintain the content of auxiliary elements (copper, manganese, cobalt, zinc) within normal limits, it is necessary to give the baby beets, yolks and fruits (apples, peaches, apricots). The child is also required to receive the necessary amount of fresh air - walks in the fresh air are required. Protect children from contact with harmful chemicals, especially volatile ones. Use medications only as prescribed by a doctor and under his supervision.

Prevention of anemia for an adult is similar to that for children. These are the same foods rich in iron and microelements, as well as an active healthy lifestyle and fresh air.

In childhood, the use of iron supplements preventively not only prevents the development of iron deficiency in the child, but also reduces the incidence of ARVI. In case of aggravated hereditary anemia, the medical prognosis directly depends on the frequency of crises and their severity.

In any situation, one must not give up and it is preferable to recognize any disease as soon as possible, at its earlier stages. Be more attentive to yourself and your loved ones. Preventive measures for posthemorrhagic anemia are not as complicated as it might seem. Just live, eat well, actively spend your time in nature with your family and friends, and this trouble will bypass you. But if something irreparable has happened and trouble has come to your home, don’t panic, call the doctors and fight with them. After all, life is beautiful and worth this struggle.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2013

Iron deficiency anemia, unspecified (D50.9)

Hematology

general information

Short description

Approved by the minutes of the meeting
Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan
No. 23 from 12/12/2013

Iron deficiency anemia (IDA)- clinical-hematological syndrome, characterized by impaired hemoglobin synthesis as a result of iron deficiency, developing against the background of various pathological (physiological) processes, and manifested by signs of anemia and sideropenia (L.I. Dvoretsky, 2004).

Protocol name:

IRON-DEFICIENCY ANEMIA

Protocol code:

ICD-10 code(s):
D 50 Iron deficiency anemia
D 50.0 Posthemorrhagic (chronic) anemia
D 50.8 Other iron deficiency anemias
D 50.9 Iron deficiency anemia, unspecified

Date of protocol development: 2013

Abbreviations used in the protocol:
ID - iron deficiency
DNA - deoxyribonucleic acid
IDA - iron deficiency anemia
IDS - iron deficiency state
CPU - color index

Protocol users: hematologist, therapist, gastroenterologist, surgeon, gynecologist

Classification

There is currently no generally accepted classification of iron deficiency anemia.

Clinical classification of iron deficiency anemia (for Kazakhstan).
In the diagnosis of iron deficiency anemia, it is necessary to highlight 3 points:

Etiological form (will be clarified after further examination)
- Due to chronic blood loss (chronic posthemorrhagic anemia)
- Due to increased iron consumption (increased iron requirement)
- Due to insufficient baseline iron levels (in newborns and young children)
- Alimentary (nutritive)
- Due to insufficient absorption in the intestines
- Due to impaired iron transport

Stages
A. Latent: decreased Fe in the blood serum, iron deficiency without clinical anemia (latent anemia)
B. Clinically developed picture of hypochromic anemia.

Severity
Light (Hb content 90-120 g/l)
Average (Hb content 70-89 g/l)
Severe (Hb content below 70 g/l)

Example: Iron deficiency anemia, post-gastroresection, stage B, severe.

Diagnostics

List of main diagnostic measures:

1. General blood test (12 parameters)
2. Biochemical blood test (total protein, bilirubin, urea, creatinine, ALT, AST, bilirubin and fractions)
3. Serum iron, ferritin, TBC, blood reticulocytes
4. General urine analysis

List of additional diagnostic measures:

1. Fluorography
2. Esophagogastroduodenoscopy,
3. Ultrasound of the abdominal cavity, kidneys,
4. X-ray examination of the gastrointestinal tract according to indications,
5. X-ray examination of the chest organs according to indications,
6. Fibercolonoscopy,
7. Sigmoidoscopy,
8. Ultrasound of the thyroid gland.
9. Sternal puncture for differential diagnosis, after consultation with a hematologist, according to indications

Diagnostic criteria*** (description of reliable signs of the disease depending on the severity of the process).

1) Complaints and anamnesis:

Information from the anamnesis:
Chronic posthemorrhagic IDA

1. Uterine bleeding . Menorrhagia of various origins, hyperpolymenorrhea (menses more than 5 days, especially when the first menstruation appears before 15 years, with a cycle of less than 26 days, the presence of blood clots for more than a day), impaired hemostasis, abortion, childbirth, uterine fibroids, adenomyosis, intrauterine contraceptives, malignant tumors .

2. Bleeding from the gastrointestinal tract. When chronic blood loss is detected, a thorough examination of the digestive tract “from top to bottom” is carried out, excluding diseases of the oral cavity, esophagus, stomach, intestines, and helminthic infestation by hookworm. In adult men and women after menopause, the main cause of iron deficiency is bleeding from the gastrointestinal tract, which can provoke: peptic ulcer, diaphragmatic hernia, tumors, gastritis (alcoholic or due to treatment with salicylates, steroids, indomethacin). Disturbances in the hemostatic system can lead to bleeding from the gastrointestinal tract.

3. Donation (in 40% of women it leads to hidden iron deficiency, and sometimes, mainly in female donors with many years of experience (more than 10 years) - it provokes the development of IDA.

4. Other blood loss : nasal, renal, iatrogenic, artificially caused by mental illness.

5. Hemorrhages in confined spaces : pulmonary hemosiderosis, glomic tumors, especially with ulceration, endometriosis.

IDA associated with increased iron requirements:
Pregnancy, lactation, puberty and intensive growth, inflammatory diseases, intense sports, treatment with vitamin B 12 in patients with B 12 deficiency anemia.
One of the most important pathogenetic mechanisms for the development of anemia in pregnant women is inadequately low production of erythropoietin. In addition to states of overproduction of proinflammatory cytokines caused by pregnancy itself, their overproduction is possible with concomitant chronic diseases (chronic infections, rheumatoid arthritis, etc.).

IDA associated with impaired iron intake
Poor nutrition with a predominance of flour and dairy products. When collecting anamnesis, it is necessary to take into account dietary habits (vegetarianism, fasting, dieting). In some patients, impaired intestinal iron absorption may be masked by common syndromes such as steatorrhea, sprue, celiac disease, or diffuse enteritis. Iron deficiency often occurs after resection of the intestine, stomach, or gastroenterostomy. Atrophic gastritis and concomitant achlorhydria can also reduce iron absorption. Poor absorption of iron can be contributed to by a decrease in the production of hydrochloric acid and a decrease in the time required for the absorption of iron. In recent years, the role of Helicobacter pylori infection in the development of IDA has been studied. It has been noted that in some cases, iron metabolism in the body during Helicobacter eradication can be normalized without additional measures.

IDA associated with impaired iron transport
These IDA are associated with congenital antransferrinemia, the presence of antibodies to transferrin, and a decrease in transferrin due to a general protein deficiency.

a. General anemic syndrome:weakness, increased fatigue, dizziness, headaches (usually in the evening), shortness of breath during exercise, palpitations, syncope, flashing “flies” before the eyes with low blood pressure, a moderate increase in temperature is often observed, often drowsiness during the day and poor falling asleep at night, irritability, nervousness, conflict, tearfulness, decreased memory and attention, decreased appetite. The severity of complaints depends on adaptation to anemia. A slow pace of anemization contributes to better adaptation.

b. Sideropenic syndrome:

- changes in the skin and its appendages(dryness, peeling, easy cracking, pallor). Hair is dull, brittle, “split”, turns gray early, falls out rapidly, changes in nails: thinning, brittleness, transverse striations, sometimes spoon-shaped concavity (koilonychia).
- Changes in mucous membranes(glossitis with atrophy of the papillae, cracks in the corners of the mouth, angular stomatitis).
- Changes in the gastrointestinal tract(atrophic gastritis, atrophy of the esophageal mucosa, dysphagia). Difficulty swallowing dry and solid foods.
- Muscular system. Myasthenia gravis (due to weakening of the sphincters, an imperative urge to urinate, the inability to hold urine when laughing, coughing, and sometimes bedwetting in girls). The consequence of myasthenia gravis can be miscarriage, complications during pregnancy and childbirth (decreased contractility of the myometrium
Predilection for unusual smells.
Perversion of taste. Expressed in the desire to eat something inedible.
- Sideropenic myocardial dystrophy- tendency to tachycardia, hypotension.
- Immune system disorders(the level of lysozyme, B-lysines, complement, some immunoglobulins decreases, the level of T- and B-lymphocytes decreases, which contributes to a high infectious morbidity in IDA and the appearance of secondary immunodeficiency of a combined nature).

2) physical examination:
. pallor of the skin and mucous membranes;
. “blueness” of the sclera due to their degenerative changes, slight yellowness of the area of ​​the nasolabial triangle, palms as a result of impaired carotene metabolism;
. koilonychia;
. cheilitis (seizures);
. vague symptoms of gastritis;
. involuntary urination (due to sphincter weakness);
. symptoms of damage to the cardiovascular system: palpitations, shortness of breath, chest pain and sometimes swelling in the legs.

3) laboratory tests

Laboratory indicators for IDA

	Laboratory indicator	Norm	Changes in IDA
1	Morphological changes in red blood cells	normocytes - 68% microcytes - 15.2% macrocytes - 16.8%	Microcytosis is combined with anisocytosis, poikilocytosis, anulocytes, plantocytes are present
2	Color index	0,86 -1,05	Hypochromia indicator less than 0.86
3	Hemoglobin content	Women - at least 120 g/l Men - at least 130 g/l	Reduced
4	MSN	27-31 pg	Less than 27 pg
5	ICSU	33-37%	Less than 33%
6	MCV	80-100 fl	Reduced
7	RDW	11,5 - 14,5%	Increased
8	Average red blood cell diameter	7.55±0.099 µm	Reduced
9	Reticulocyte count	2-10:1000	Not changed
10	Effective erythropoiesis coefficient	0.06-0.08x10 12 l/day	Not changed or reduced
11	Serum iron	Women - 12-25 µml/l Men -13-30 µmol/l	Reduced
12	Total iron binding capacity of blood serum	30-85 µmol/l	Promoted
13	Latent iron binding capacity of serum	Less than 47 µmol/l	Above 47 µmol/l
14	Transferrin saturation with iron	16-15%	Reduced
15	Desferal test	0.8-1.2 mg	Decrease
16	Content of protoporphyrins in erythrocytes	18-89 µmol/l	Increased
17	Iron painting	Sideroblasts are present in the bone marrow	Disappearance of sideroblasts in punctate
18	Ferritin level	15-150 µg/l	Decrease

4) instrumental studies (x-ray signs, endoscopy - picture).
In order to identify sources of blood loss and pathology of other organs and systems:
- X-ray examination of the gastrointestinal tract according to indications,
- X-ray examination of the chest organs according to indications,
- fibrocolonoscopy,
- sigmoidoscopy,
- Ultrasound of the thyroid gland.
- Sternal puncture for differential diagnosis

5) indications for consultation with specialists:
gastroenterologist - bleeding from the gastrointestinal tract;
dentist - bleeding from gums,
ENT - nosebleeds,
oncologist - a malignant lesion that causes bleeding,
nephrologist - exclusion of kidney diseases,
phthisiatrician - bleeding due to tuberculosis,
pulmonologist - blood loss due to diseases of the bronchopulmonary system, gynecologist - bleeding from the genital tract,
endocrinologist - decreased thyroid function, presence of diabetic nephropathy,
hematologist - to exclude diseases of the blood system, ineffectiveness of ferrotherapy
proctologist - rectal bleeding,
infectious disease specialist - if there are signs of helminthiasis.

Differential diagnosis

Criteria	ZhDA	MDS (RA)	B12-deficient	Hemolytic anemia
				Hereditary	AIGA
Age	Most often young, under 60 years old	Over 60 years old	Over 60 years old	-	After 30 years
Shape of red blood cells	Anisocytosis, poikilocytosis	Megalocytes	Megalocytes	Sphero-, ovalocytosis	Norm
Color index	Reduced	Normal or elevated	Promoted	Norm	Norm
Price-Jones curve	Norm	Shift right or normal	Shift right	Norm or shift right	Shift left
Lifespan of Erythr.	Norm	Normal or shortened	Shortened	Shortened	Shortened
Coombs test	Negative	Negative sometimes positive	Negative	Negative	Positive
Osmotic resistance Er.	Norm	Norm	Norm	Promoted	Norm
Peripheral blood reticulocytes	Relates. increase, absolute decrease	Decreased or increased	Demoted on days 5-7 of treatment, reticulocyte crisis	Increased	Increase
Peripheral blood leukocytes	Norm	Reduced	Possible downgrade	Norm	Norm
Peripheral blood platelets	Norm	Reduced	Possible downgrade	Norm	Norm
Serum iron	Reduced	Increased or normal	Increased	Increased or normal	Increased or normal
Bone marrow	Increase in polychromatophiles	Hyperplasia of all hematopoietic germs, signs of cell dysplasia	Megaloblasts	Increased erythropoiesis with increasing mature forms
Blood bilirubin	Norm	Norm	Possible promotion	Increase in indirect bilirubin fraction
Urobilin urine	Norm	Norm	Possible appearance	Persistent increase in urine urobilin

Differential diagnosis of iron deficiency anemia is carried out with other hypochromic anemias caused by impaired hemoglobin synthesis. These include anemia associated with impaired porphyrin synthesis (anemia due to lead poisoning, congenital disorders of porphyrin synthesis), as well as thalassemia. Hypochromic anemia, unlike iron deficiency anemia, occurs with a high content of iron in the blood and depot, which is not used for the formation of heme (sideroachresia); in these diseases there are no signs of tissue iron deficiency.
The differential sign of anemia caused by impaired porphyrin synthesis is hypochromic anemia with basophilic punctation of erythrocytes, reticulocytes, enhanced erythropoiesis in the bone marrow with a large number of sideroblasts. Thalassemia is characterized by a target-like shape and basophilic punctation of erythrocytes, reticulocytosis and the presence of signs of increased hemolysis

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment goals:
- Correction of iron deficiency.
- Comprehensive treatment of anemia and complications associated with it.
- Elimination of hypoxic conditions.
- Normalization of hemodynamics, systemic, metabolic and organ disorders.

Treatment tactics***:

non-drug treatment
In case of iron deficiency anemia, the patient is advised to eat a diet rich in iron. The maximum amount of iron that can be absorbed from food in the gastrointestinal tract is 2 g per day. Iron from animal products is absorbed in the intestines in much larger quantities than from plant products. Bivalent iron, which is part of heme, is best absorbed. Meat iron is absorbed better, but liver iron is absorbed worse, since iron in the liver is contained mainly in the form of ferritin, hemosiderin, and also in the form of heme. Iron is absorbed in small quantities from eggs and fruits. The patient is recommended the following foods containing iron: beef, fish, liver, kidneys, lungs, eggs, oatmeal, buckwheat, beans, porcini mushrooms, cocoa, chocolate, greens, vegetables, peas, beans, apples, wheat, peaches, raisins , prunes, herring, hematogen. It is advisable to take kumis in a daily dose of 0.75-1 l, with good tolerance - up to 1.5 l. In the first two days, the patient is given no more than 100 ml of kumis at each dose; from the 3rd day, the patient takes 250 ml 3-4 times a day. It is better to take kumys 1 hour before and 1 hour after breakfast, 2 hours before and 1 hour after lunch and dinner.
In the absence of contraindications (diabetes mellitus, obesity, allergies, diarrhea), the patient should be recommended honey. Honey contains up to 40% fructose, which helps increase the absorption of iron in the intestines. Iron is best absorbed from veal (22%), from fish (11%); 3% of iron is absorbed from eggs, beans, and fruits, and 1% from rice, spinach, and corn.

drug treatment
List separately
- list of essential medicines
- list of additional medicines
***in these sections it is necessary to provide a link to a source that has a good evidence base, indicating the level of reliability. Links should be indicated in the form of square brackets, numbered as they appear. This source must be indicated in the list of references under the appropriate number.

Treatment of IDA should include the following steps:

1. Relief of anemia.
   B. Saturation therapy (restoration of iron reserves in the body).
   B. Maintenance therapy.

The daily dose for the prevention of anemia and treatment of mild forms of the disease is 60-100 mg of iron, and for the treatment of severe anemia - 100-120 mg of iron (for iron sulfate).
The inclusion of ascorbic acid in iron salt preparations improves its absorption. For iron (III) hydroxide polymaltose, the dose may be higher, approximately 1.5 times relative to the latter, because The drug is non-ionic and is tolerated significantly better than iron salts, while only the amount of iron that the body needs is absorbed and only through the active route.
It should be noted that iron is better absorbed when the stomach is “empty”, so it is recommended to take the drug 30-60 minutes before meals. With adequate administration of iron supplements in a sufficient dose, a rise in reticulocytes is noted on days 8-12, and the Hb content increases by the end of the 3rd week. Normalization of red blood counts occurs only after 5-8 weeks of treatment.

All iron preparations are divided into two groups:
1. Ionic iron-containing preparations (salt, polysaccharide compounds of ferrous iron - Sorbifer, Ferretab, Tardiferon, Maxifer, Ranferon-12, Aktiferin, etc.).
2. Nonionic compounds, which include ferric iron preparations, represented by the iron-protein complex and the hydroxide-polymaltose complex (Maltofer). Iron (III)-hydroxide polymaltose complex (Venofer, Cosmofer, Ferkail)

Table. Basic iron preparations for oral administration

A drug	Additional components	Dosage form	Amount of iron, mg
Monocomponent drugs
Aristopheron	ferrous sulfate	syrup - 200 ml, 5 ml - 200 mg
Ferronal	ferrous gluconate	tab., 300 mg	12%
Ferrogluconate	ferrous gluconate	tab., 300 mg	12%
Hemophere prolongatum	ferrous sulfate	tab., 325 mg	105 mg
Iron wine	iron sucrose	solution, 200 ml 10 ml - 40 mg
Heferol	ferrous fumarate	capsules, 350 mg	100 mg
Combination drugs
Aktiferin	Ferrous sulfate, D,L-serine ferrous sulfate, D,L-serine, glucose, fructose ferrous sulfate, D,L-serine, glucose, fructose, potassium sorbate	caps., 0.11385 g syrup, 5 ml-0.171 g drops, 1 ml - 0.0472 g	0.0345 g 0.034 g 0.0098 g
Sorbifer - durules	ferrous sulfate, ascorbic acid acid	tab., 320 mg	100 mg
Ferrstab		tab., 154 mg	33%
Folfetab	Ferrous fumarate, folic acid	tab., 200 mg	33%
Ferroplect	ferrous sulfate, ascorbic acid acid	tab., 50 mg	10 mg
Ferroplex	ferrous sulfate, ascorbic acid acid	tab., 50 mg	20%
Fefol	ferrous sulfate, folic acid	tab., 150 mg	47 mg
Ferro-foil	ferrous sulfate, folic acid, cyanocobalamin	caps., 100 mg	20%
Tardiferon - retard	ferrous sulfate, ascorbic acid	dragee, 256.3 mg	80 mg
	acid, mucoproteosis
Gyno-tardiferon	ferrous sulfate, ascorbic acid acid, mucoproteosis, folic acid	dragee, 256.3 mg	80 mg
2Macrofer	Ferrous gluconate, folic acid	effervescent tablets, 625 mg	12%
Fenyuls	ferrous sulfate, ascorbic acid acid, nicotinamide, vitamins Group B	caps.,	45 mg
Irovit	ferrous sulfate, ascorbic acid acid, folic acid, cyanocobalamin, lysine monohydro- chloride	caps., 300 mg	100 mg
Ranferon-12	Ferrous fumarate, ascorbic acid, folic acid, cyanocobalamin, zinc sulfate	Caps., 300 mg	100 mg
Totema	Iron gluconate, manganese gluconate, copper gluconate	Ampoules with drinking solution	50 mg
Globiron	Ferrous fumarate, folic acid, cyanocobalamin, pyridoxine, sodium docusate	Caps., 300 mg	100 mg
Gemsineral-TD	Ferrous fumarate, folic acid, cyanocobalamin	Caps., 200 mg	67 mg
Ferramin-Vita	Ferrous aspartate, ascorbic acid, folic acid, cyanocobalamin, zinc sulfate	Table, 60 mg
Maltofer		Drops, syrup, 10 mg Fe in 1 ml; Table chewable 100 mg
Maltofer Fall	polymaltose hydroxyl iron complex, folic acid	Table chewable 100 mg
Ferrum Lek	polymaltose hydroxyl iron complex	Table chewable 100 mg

To relieve mild IDA:
Sorbifer 1 tablet. x 2 rub. per day 2-3 weeks, Maxifer 1 tablet. x 2 times a day, 2-3 weeks, Maltofer 1 tablet 2 times a day - 2-3 weeks, Ferrum-lek 1 tablet x 3 r. in the village 2-3 weeks;
Moderate severity: Sorbifer 1 tablet. x 2 rub. per day 1-2 months, Maxifer 1 tablet. x 2 times a day, 1-2 months, Maltofer 1 tablet 2 times a day - 1-2 months, Ferrum-lek 1 tablet x 3 r. in the village 1-2 months;
Severe severity: Sorbifer 1 tablet. x 2 rub. per day 2-3 months, Maxifer 1 tablet. x 2 times a day, 2-3 months, Maltofer 1 tablet 2 times a day - 2-3 months, Ferrum-lek 1 tablet x 3 r. in the village 2-3 months.
Of course, the duration of therapy is influenced by the hemoglobin level during ferrotherapy, as well as the positive clinical picture!

Table. Iron preparations for parenteral administration.

Trade name	INN	Dosage form	Amount of iron, mg
Venofer IV	Iron III hydroxide sucrose complex	Ampoules 5.0	100 mg
Ferkail v/m	Iron III dextran	Ampoules 2.0	100 mg
Cosmopher v/m, v/v		Ampoules 2.0	100 mg
Novofer-D intramuscularly, intravenously	Iron III hydroxide-dextran complex	Ampoules 2.0	100 mg/2ml

Indications for parenteral administration of iron supplements:
. Intolerance to iron supplements for oral administration;
. Impaired absorption of iron;
. Peptic ulcer of the stomach and duodenum during exacerbation;
. Severe anemia and the vital need to quickly replenish iron deficiency, for example, preparation for surgery (refusal of hemocomponent therapy)
For parenteral administration, ferric iron preparations are used.
The course dose of iron preparations for parenteral administration is calculated using the formula:
A = 0.066 M (100 - 6 Nb),
where A is the course dose, mg;
M—patient’s body weight, kg;
Hb—Hb content in blood, g/l.

IDA treatment regimen:
1. If the hemoglobin level is 109-90 g/l, hematocrit is 27-32%, prescribe a combination of drugs:

A diet that includes iron-rich foods - beef tongue, rabbit meat, chicken, porcini mushrooms, buckwheat or oatmeal, legumes, cocoa, chocolate, prunes, apples;

Salts, polysaccharide compounds of ferrous iron, iron (III)-hydroxide polymaltose complex in a total daily dose of 100 mg (oral administration) for 1.5 months with monitoring of a general blood test once a month, if necessary, extending the course of treatment to 3 months;

Ascorbic acid 2 dr. x 3 r. in the village 2 weeks

2. If the hemoglobin level is below 90 g/l, the hematocrit is below 27%, consult a hematologist.
Salt or polysaccharide compounds of ferrous iron or iron (III)-hydroxide polymaltose complex in a standard dosage. In addition to the previous therapy, prescribe iron (III)-hydroxide polymaltose complex (200 mg/10 ml) intravenously every other day, the amount of administered iron should be calculated according to the formula given in the manufacturer’s instructions or iron III dextran (100 mg/2 ml) once every day, intramuscularly (calculation according to the formula), with individual selection of the course depending on hematological parameters, at this moment the intake of oral iron supplements is temporarily stopped;

3. When the hemoglobin level is normalized to more than 110 g/l and hematocrit to more than 33%, prescribe a combination of preparations of salt or polysaccharide compounds of divalent iron or iron (III)-hydroxide polymaltose complex 100 mg once a week for 1 month, under the control of hemoglobin levels, ascorbic acid 2 dr. x 3 r. per day 2 weeks (not applicable for pathologies of the gastrointestinal tract - erosion and ulcers of the esophagus, stomach), folic acid 1 tablet. x 2 rub. in the village for 2 weeks.

4. If the hemoglobin level is less than 70 g/l, inpatient treatment in the hematology department, if acute gynecological or surgical pathology is excluded. Mandatory preliminary examination by a gynecologist and surgeon.

In case of severe anemic and circulatory-hypoxic syndromes, leukofiltered erythrocyte suspension, further transfusions strictly according to absolute indications, according to the Order of the Minister of Health of the Republic of Kazakhstan dated July 26, 2012 No. 501. On amendments to the order of the acting. Minister of Health of the Republic of Kazakhstan dated November 6, 2009 No. 666 “On approval of the Nomenclature, Rules for the procurement, processing, storage, sale of blood and its components, as well as Rules for the storage, transfusion of blood, its components and preparations”

In the preoperative period, in order to quickly normalize hematological parameters, transfusion of leukofiltered erythrocyte suspension, according to Order No. 501;

Salt or polysaccharide compounds of divalent iron or iron (III)-hydroxide polymaltose complex (200 mg/10 ml) intravenously every other day according to calculations according to the instructions and under the control of hematological parameters.

For example, a scheme for calculating the amount of administered drug relative to Cosmofer:
Total dose (Fe mg) = body weight (kg) x (required Hb - actual Hb) (g/l) x 0.24 + 1000 mg (Fe reserve). Factor 0.24 = 0.0034 (iron content in Hb is 0.34%) x 0.07 (blood volume 7% of body weight) x 1000 (transition from g to mg). Course dose in ml (for iron deficiency anemia) in terms of body weight (kg) and depending on Hb indicators (g/l), which corresponds to:
60, 75, 90, 105 g/l:
60 kg - 36, 32, 27, 23 ml, respectively;
65 kg - 38, 33, 29, 24 ml, respectively;
70 kg - 40, 35, 30, 25 ml, respectively;
75 kg - 42, 37, 32, 26 ml, respectively;
80 kg - 45, 39, 33, 27 ml, respectively;
85 kg - 47, 41, 34, 28 ml, respectively;
90 kg - 49, 42, 36, 29 ml, respectively.

If necessary, treatment is described in stages: emergency care, outpatient, inpatient.

Other treatments- No

Surgical intervention

Indications for surgical treatment are ongoing bleeding, increasing anemia, due to reasons that cannot be eliminated by drug therapy.

Prevention

Primary prevention carried out in groups of people who do not currently have anemia, but there are circumstances predisposing to the development of anemia:
. pregnant and breastfeeding women;
. teenage girls, especially those with heavy menstruation;
. donors;
. women with heavy and prolonged menstruation.

Prevention of iron deficiency anemia in women with heavy and prolonged menstruation.
2 courses of preventive therapy are prescribed for a duration of 6 weeks (the daily dose of iron is 30-40 mg) or after menstruation for 7-10 days every month for a year.
Prevention of iron deficiency anemia in donors and children of sports schools.
1-2 courses of preventive treatment are prescribed for 6 weeks in combination with an antioxidant complex.
During periods of intense growth in boys, iron deficiency anemia may develop. At this time, preventive treatment with iron supplements should also be carried out.

Secondary prevention is performed for persons with previously cured iron deficiency anemia in the presence of conditions that threaten the development of relapse of iron deficiency anemia (heavy menstruation, uterine fibroids, etc.).

For these groups of patients, after treatment of iron deficiency anemia, a preventive course lasting 6 weeks is recommended (daily dose of iron - 40 mg), then two 6-week courses per year or taking 30-40 mg of iron daily for 7-10 days after menstruation are given. In addition, you must consume at least 100 g of meat daily.

All patients with iron deficiency anemia, as well as persons with risk factors for this pathology, must be registered with a general practitioner in the clinic at their place of residence, with a mandatory general blood test and serum iron testing at least 2 times a year. At the same time, clinical observation is also carried out taking into account the etiology of iron deficiency anemia, i.e. The patient is being monitored for a disease that has caused iron deficiency anemia.

Further management
Clinical blood tests should be performed monthly. In case of severe anemia, laboratory monitoring is carried out every week; in the absence of positive dynamics of hematological parameters, an in-depth hematological and general clinical examination is indicated.

Information

Sources and literature

1. Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
   1. List of references: 1. WHO. Official annual report. Geneva, 2002. 2. Iron deficiency anemia assessment, prevention and control. A guide for program managers - Geneva: World Health Organization, 2001 (WHO/NHD/01.3). 3. Dvoretsky L.I. WAITING. Newdiamid-AO. M.: 1998. 4. Kovaleva L. Iron deficiency anemia. M.: Doctor. 2002; 12:4-9. 5. G. Perewusnyk, R. Huch, A. Huch, C. Breymann. British Journal of Nutrition. 2002; 88: 3-10. 6. Strai S.K.S., Bomford A., McArdle H.I. Iron transport across cell membranes: molecular understanding of duodenal and placental iron uptake. Best Practice & Research Clin Haem. 2002; 5:2:243-259. 7. Schaeffer R.M., Gachet K., Huh R., Krafft A. Iron letter: recommendations for the treatment of iron deficiency anemia. Hematology and Transfusiology 2004; 49 (4): 40-48. 8. Dolgov V.V., Lugovskaya S.A., Morozova V.T., Pochtar M.E. Laboratory diagnosis of anemia. M.: 2001; 84. 9. Novik A.A., Bogdanov A.N. Anemia (from A to Z). Guide for doctors / ed. Academician Yu.L. Shevchenko. – St. Petersburg: “Neva”, 2004. – 62-74 p. 10. Papayan A.V., Zhukova L.Yu. Anemia in children: hands. For doctors. – St. Petersburg: Peter, 2001. – 89-127 p. 11. Alekseev N.A. Anemia. – St. Petersburg: Hippocrates. – 2004. – 512 p. 12. Lewis S.M., Bain B., Bates I. Practical and laboratory hematology / trans. from English edited by A.G. Rumyantseva. - M.: GEOTAR-Media, 2009. - 672 p.

Information

List of protocol developers indicating qualification data

A.M. Raisova - head dept. Therapy, Ph.D.
O.R. Khan - assistant at the Department of Postgraduate Therapy, hematologist

Disclosure of no conflict of interest: No

Reviewers:

Specifying the conditions for reviewing the protocol: every 2 years.

Attached files

Attention!

• By self-medicating, you can cause irreparable harm to your health.
• The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact a medical facility if you have any illnesses or symptoms that concern you.
• The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
• The MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are exclusively information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
• The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.