ICD code: anemia. Iron-deficiency anemia. D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere

Anemia is a clinical and hematological syndrome characterized by a decrease in the number of red blood cells and hemoglobin in the blood. The most diverse pathological processes can serve as the basis for the development of anemic conditions, and therefore anemia should be considered as one of the symptoms of the underlying disease. The prevalence of anemia varies significantly, ranging from 0.7 to 6.9%. The cause of anemia can be one of three factors or a combination of them: blood loss, insufficient production of red blood cells, or increased destruction of red blood cells (hemolysis).

Among various anemic conditions iron deficiency anemia are the most common and account for about 80% of all anemias.

Iron-deficiency anemia- hypochromic microcytic anemia, which develops as a result of an absolute decrease in iron reserves in the body. Iron deficiency anemia occurs, as a rule, with chronic blood loss or insufficient intake of iron into the body.

According to World Organization healthcare, every 3rd woman and every 6th man in the world (200 million people) suffer from iron deficiency anemia.

Iron metabolism
Iron is an essential biometal that plays an important role in the functioning of cells in many body systems. Biological significance iron is determined by its ability to reversibly oxidize and reduce. This property ensures the participation of iron in the processes of tissue respiration. Iron makes up only 0.0065% of body weight. The body of a man weighing 70 kg contains approximately 3.5 g (50 mg/kg body weight) of iron. The iron content in the body of a woman weighing 60 kg is approximately 2.1 g (35 mg/kg body weight). Iron compounds have different structures, have unique functional activity and play an important biological role. The most important iron-containing compounds include: hemoproteins, structural component which is heme (hemoglobin, myoglobin, cytochromes, catalase, peroxidase), non-heme group enzymes (succinate dehydrogenase, acetyl-CoA dehydrogenase, xanthine oxidase), ferritin, hemosiderin, transferrin. Iron is part of complex compounds and is distributed in the body as follows:
- heme iron - 70%;
- iron depot - 18% (intracellular accumulation in the form of ferritin and hemosiderin);
- functioning iron - 12% (myoglobin and iron-containing enzymes);
- transported iron - 0.1% (iron bound to transferrin).

There are two types of iron: heme and non-heme. Heme iron is part of hemoglobin. It is contained only in a small part of the diet (meat products), is well absorbed (20-30%), its absorption is practically not affected by other food components. Non-heme iron is found in free ionic form - ferrous (Fe II) or ferric iron (Fe III). Most of dietary iron- non-heme (found mainly in vegetables). The degree of its absorption is lower than that of heme and depends on a number of factors. Only divalent non-heme iron is absorbed from food. To “convert” ferric iron into divalent iron, a reducing agent is needed, the role of which in most cases is played by ascorbic acid(vitamin C). During absorption in the cells of the intestinal mucosa, ferrous iron Fe2+ is converted into oxide Fe3+ and binds to a special carrier protein - transferrin, which transports iron to hematopoietic tissues and sites of iron deposition.

Iron accumulation is carried out by the proteins ferritin and hemosiderin. If necessary, iron can be actively released from ferritin and used for erythropoiesis. Hemosiderin is a derivative of ferritin with a higher iron content. Iron is released slowly from hemosiderin. Incipient (prelatent) iron deficiency can be determined by a reduced concentration of ferritin even before the depletion of iron stores, while still maintaining normal concentrations of iron and transferrin in the blood serum.

What causes iron deficiency anemia:

The main etiopathogenetic factor of development iron deficiency anemia- iron deficiency. The most common causes of iron deficiency conditions are:
1. loss of iron during chronic bleeding (most common reason, reaching 80%):
- bleeding from gastrointestinal tract: peptic ulcer, erosive gastritis, varicose veins esophageal veins, colon diverticula, hookworm infestations, tumors, UC, hemorrhoids;
- long and heavy menstruation, endometriosis, fibroids;
- macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis disease, polycystic kidney disease, kidney and bladder tumors;
- nosebleeds, pulmonary bleeding;
-- blood loss during hemodialysis;
-- uncontrolled donation;
2. insufficient absorption of iron:
-- resection of the small intestine;
- chronic enteritis;
- malabsorption syndrome;
-- intestinal amyloidosis;
3. increased need for iron:
-- intensive growth;
-- pregnancy;
- period of breastfeeding;
- playing sports;
4. insufficient intake of iron from food:
-- newborns;
-- Small children;
-- vegetarianism.

Pathogenesis (what happens?) during Iron deficiency anemia:

Pathogenetically, the development of iron deficiency can be divided into several stages:
1. prelatent iron deficiency (insufficient accumulation) - there is a decrease in ferritin levels and a decrease in iron content in the bone marrow, increased iron absorption;
2. latent iron deficiency (iron deficiency erythropoiesis) - serum iron is further reduced, transferrin concentration increases, and the content of sideroblasts in the bone marrow decreases;
3. severe iron deficiency = iron deficiency anemia - the concentration of hemoglobin, red blood cells and hematocrit further decreases.

Symptoms of Iron Deficiency Anemia:

During the period of hidden iron deficiency, many subjective complaints appear and Clinical signs, characteristic of iron deficiency anemia. Patients note general weakness, malaise, and decreased performance. Already during this period, there may be a perversion of taste, dryness and tingling of the tongue, difficulty swallowing with a feeling foreign body sore throat, palpitations, shortness of breath.
An objective examination of patients reveals “minor symptoms of iron deficiency”: atrophy of the tongue papillae, cheilitis, dry skin and hair, brittle nails, burning and itching of the vulva. All these signs of impaired trophism of epithelial tissues are associated with tissue sideropenia and hypoxia.

Patients with iron deficiency anemia report general weakness, fatigue, difficulty concentrating, and sometimes drowsiness. Appear headache, dizziness. Severe anemia may cause fainting. These complaints, as a rule, do not depend on the degree of decrease in hemoglobin, but on the duration of the disease and the age of the patients.

Iron deficiency anemia is also characterized by changes in the skin, nails and hair. The skin is usually pale, sometimes with a slight greenish tint (chlorosis) and with an easy blush on the cheeks, it becomes dry, flabby, peels, and cracks easily form. Hair loses its shine, turns grey, thins, breaks easily, thins and turns gray early. Changes in nails are specific: they become thin, matte, flattened, easily peel and break, and striations appear. With pronounced changes, the nails acquire a concave, spoon-shaped shape (koilonychia). Patients with iron deficiency anemia experience muscle weakness, which is not observed in other types of anemia. It is classified as a manifestation of tissue sideropenia. Atrophic changes occur in the mucous membranes of the digestive canal, respiratory organs, and genital organs. Damage to the mucous membrane of the digestive canal is a typical sign of iron deficiency conditions.
There is a decrease in appetite. There is a need for sour, spicy, salty foods. In more severe cases, distortions of smell and taste (pica chlorotica) are observed: eating chalk, lime, raw cereals, pogophagia (craving for eating ice). Signs of tissue sideropenia quickly disappear after taking iron supplements.

Diagnosis of Iron Deficiency Anemia:

Basic landmarks in laboratory diagnostics iron deficiency anemia the following:
1. The average hemoglobin content in an erythrocyte in picograms (normal 27-35 pg) is reduced. To calculate it, the color index is multiplied by 33.3. For example, when color index 0.7 x 33.3 hemoglobin content is 23.3 pg.
2. The average concentration of hemoglobin in the erythrocyte is reduced; Normally it is 31-36 g/dl.
3. Hypochromia of erythrocytes is determined by microscopy of a peripheral blood smear and is characterized by an increase in the zone of central clearing in the erythrocyte; Normally, the ratio of central clearing to peripheral darkening is 1:1; for iron deficiency anemia - 2+3:1.
4. Microcytosis of erythrocytes - reduction in their size.
5. Coloring of erythrocytes of different intensity - anisochromia; the presence of both hypo- and normochromic red blood cells.
6. Different shape erythrocytes - poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and a period of ferrotherapy) in iron deficiency anemia remains normal.
8. The leukocyte count is also within normal limits (except in cases of blood loss or cancer pathology).
9. The platelet count often remains within normal limits; moderate thrombocytosis is possible with blood loss at the time of examination, and the platelet count decreases when the basis of iron deficiency anemia is blood loss due to thrombocytopenia (for example, with DIC syndrome, Werlhof's disease).
10. Reducing the number of siderocytes until they disappear (a siderocyte is an erythrocyte containing iron granules). In order to standardize the production of peripheral blood smears, it is recommended to use special automatic devices; the resulting monolayer of cells increases the quality of their identification.

Blood chemistry:
1. Decrease in iron content in blood serum (normally in men 13-30 µmol/l, in women 12-25 µmol/l).
2. The total life-value percentage is increased (reflects the amount of iron that can be bound due to free transferrin; the normal level of total life-value percentage is 30-86 µmol/l).
3. Study of transferrin receptors using the enzyme immunoassay method; their level is increased in patients with iron deficiency anemia (in patients with anemia chronic diseases- normal or reduced, despite similar indicators of iron metabolism.
4. The latent iron-binding capacity of blood serum is increased (determined by subtracting the serum iron content from the TLC indicators).
5. The percentage of transferrin saturation with iron (the ratio of the serum iron index to the total life-saving value; normally 16-50%) is reduced.
6. The level of serum ferritin is also reduced (normally 15-150 mcg/l).

At the same time, in patients with iron deficiency anemia, the number of transferrin receptors is increased and the level of erythropoietin in the blood serum is increased (compensatory reactions of hematopoiesis). The volume of erythropoietin secretion is inversely proportional to the oxygen transport capacity of the blood and directly proportional to the oxygen demand of the blood. It should be taken into account that serum iron levels are higher in the morning; before and during menstruation it is higher than after menstruation. The iron content in blood serum in the first weeks of pregnancy is higher than in its last trimester. Serum iron levels increase on days 2-4 after treatment with iron-containing drugs and then decrease. Significant consumption of meat products on the eve of the study is accompanied by hypersideremia. These data must be taken into account when assessing the results of serum iron studies. It is equally important to follow the technique laboratory research, rules for blood sampling. Thus, the tubes in which blood is collected must first be washed with hydrochloric acid and double-distilled water.

Myelogram study reveals a moderate normoblastic reaction and a sharp decline content of sideroblasts (erythrokaryocytes containing iron granules).

Iron reserves in the body are judged by the results of the desferal test. U healthy person after intravenous administration 500 mg of desferal is excreted in the urine from 0.8 to 1.2 mg of iron, while in a patient with iron deficiency anemia, iron excretion is reduced to 0.2 mg. The new domestic drug defericolixam is identical to desferal, but circulates in the blood longer and therefore more accurately reflects the level of iron reserves in the body.

Taking into account the level of hemoglobin, iron deficiency anemia, like other forms of anemia, is divided into severe, moderate and mild degree. With mild iron deficiency anemia, the hemoglobin concentration is below normal, but more than 90 g/l; with moderate iron deficiency anemia, the hemoglobin content is less than 90 g/l, but more than 70 g/l; with severe iron deficiency anemia, the hemoglobin concentration is less than 70 g/l. However, clinical signs of the severity of anemia (symptoms of a hypoxic nature) do not always correspond to the severity of anemia according to laboratory criteria. Therefore, a classification of anemia according to the severity of clinical symptoms has been proposed.

Based on clinical manifestations, there are 5 degrees of severity of anemia:
1. anemia without clinical manifestations;
2. anemic syndrome moderate severity;
3. severe anemic syndrome;
4. anemic precoma;
5. anemic coma.

Moderate severity of anemia is characterized by general weakness, specific signs (for example, sideropenic or signs of vitamin B12 deficiency); with a pronounced degree of severity of anemia, palpitations, shortness of breath, dizziness, etc. appear. Precomatose and comatose states can develop in a matter of hours, which is especially typical for megaloblastic anemia.

Modern clinical studies show that laboratory and clinical heterogeneity is observed among patients with iron deficiency anemia. Thus, in some patients with signs of iron deficiency anemia and concomitant inflammatory and infectious diseases the level of serum and erythrocyte ferritin does not decrease, however, after the exacerbation of the underlying disease is eliminated, their content drops, which indicates the activation of macrophages in the processes of iron consumption. In some patients, the level of erythrocyte ferritin even increases, especially in patients with long-term iron deficiency anemia, which leads to ineffective erythropoiesis. Sometimes there is an increase in the level of serum iron and erythrocyte ferritin, a decrease in serum transferrin. It is assumed that in these cases the process of iron transfer to heme-synthesizing cells is disrupted. In some cases, a deficiency of iron, vitamin B12 and folic acid is simultaneously determined.

Thus, even the level of serum iron does not always reflect the degree of iron deficiency in the body in the presence of other signs of iron deficiency anemia. Only the level of THC in iron deficiency anemia is always increased. Therefore, not a single biochemical indicator, incl. OZHSS cannot be considered as absolute diagnostic criterion with iron deficiency anemia. At the same time, the morphological characteristics of peripheral blood erythrocytes and computer analysis of the main parameters of erythrocytes are decisive in the screening diagnosis of iron deficiency anemia.

Diagnosis of iron deficiency conditions is difficult in cases where the hemoglobin level remains normal. Iron deficiency anemia develops in the presence of the same risk factors as for iron deficiency anemia, as well as in individuals with an increased physiological need for iron, especially in premature infants. early age, in adolescents with a rapid increase in height and body weight, in blood donors, with nutritional dystrophy. In the first stage of iron deficiency clinical manifestations are absent, and iron deficiency is determined by the content of hemosiderin in bone marrow macrophages and by the absorption of radioactive iron in the gastrointestinal tract. At the second stage (latent iron deficiency), an increase in the concentration of protoporphyrin in erythrocytes is observed, the number of sideroblasts decreases, morphological signs appear (microcytosis, hypochromia of erythrocytes), the average content and concentration of hemoglobin in erythrocytes decreases, the level of serum and erythrocyte ferritin, and transferrin saturation with iron decrease. The hemoglobin level at this stage remains quite high, and clinical signs are characterized by a decrease in tolerance to physical activity. The third stage is manifested by obvious clinical and laboratory signs of anemia.

Examination of patients with iron deficiency anemia
To exclude anemia that has common features with iron deficiency anemia, and identifying the cause of iron deficiency requires a complete clinical examination of the patient:

General blood analysis with the obligatory determination of the number of platelets, reticulocytes, and the study of erythrocyte morphology.

Blood chemistry: determination of the level of iron, TLC, ferritin, bilirubin (bound and free), hemoglobin.

In all cases it is necessary examine bone marrow aspirate before prescribing vitamin B12 (primarily for differential diagnosis with megaloblastic anemia).

To identify the cause of iron deficiency anemia in women, a preliminary consultation with a gynecologist is required to exclude diseases of the uterus and its appendages, and in men, an examination by a proctologist to exclude bleeding hemorrhoids and a urologist to exclude pathology of the prostate gland.

There are known cases of extragenital endometriosis, for example in respiratory tract. In these cases, hemoptysis is observed; fiberoptic bronchoscopy with histological examination of a biopsy of the bronchial mucosa makes it possible to establish a diagnosis.

The examination plan also includes x-ray and endoscopic examination of the stomach and intestines to exclude ulcers, tumors, incl. glomic, as well as polyps, diverticulum, Crohn's disease, ulcerative colitis etc. If pulmonary siderosis is suspected, X-ray and tomography of the lungs and sputum examination for alveolar macrophages containing hemosiderin are performed; in rare cases it is necessary histological examination lung biopsy. If kidney pathology is suspected, a general urine test, blood serum testing for urea and creatinine are required, and, if indicated, an ultrasound and x-ray examination of the kidneys. In some cases, it is necessary to exclude endocrine pathology: myxedema, in which iron deficiency can develop secondary to iron deficiency small intestine; polymyalgia rheumatica - rare disease connective tissue in older women (less often in men), it is characterized by pain in the muscles of the shoulder or pelvic girdle without any objective changes in them, and in a blood test - anemia and an increase in ESR.

Differential diagnosis of iron deficiency anemia
When diagnosing iron deficiency anemia, it is necessary to carry out a differential diagnosis with other hypochromic anemias.

Iron redistribution anemia is a fairly common pathology and in terms of frequency of development it ranks second among all anemias (after iron deficiency anemia). It develops in acute and chronic infectious and inflammatory diseases, sepsis, tuberculosis, rheumatoid arthritis, liver diseases, oncological diseases, IHD, etc. The mechanism of development of hypochromic anemia in these conditions is associated with the redistribution of iron in the body (it is located mainly in the depot) and a violation of the mechanism of reutilization of iron from the depot. In the above diseases, activation of the macrophage system occurs, when macrophages, under activation conditions, firmly retain iron, thereby disrupting the process of its reutilization. IN general analysis blood there is a moderate decrease in hemoglobin (<80 г/л).

The main differences from iron deficiency anemia are:
- increased level of serum ferritin, which indicates an increased iron content in the depot;
- serum iron levels may remain within normal limits or be moderately reduced;
- TIHR remains within normal values ​​or decreases, which indicates the absence of serum Fe starvation.

Iron-saturated anemia develops as a result of a violation of heme synthesis, which is caused by heredity or can be acquired. Heme is formed from protoporphyrin and iron in erythrokaryocytes. In iron-saturated anemia, the activity of enzymes involved in the synthesis of protoporphyrin occurs. The consequence of this is a violation of heme synthesis. Iron, which was not used for heme synthesis, is deposited in the form of ferritin in macrophages of the bone marrow, as well as in the form of hemosiderin in the skin, liver, pancreas, and myocardium, resulting in the development of secondary hemosiderosis. A general blood test will record anemia, erythropenia, and a decrease in color index.

Indicators of iron metabolism in the body are characterized by an increase in the concentration of ferritin and serum iron levels, normal indicators of life-saving blood test, and an increase in transferrin saturation with iron (in some cases reaching 100%). Thus, the main biochemical indicators that allow us to assess the state of iron metabolism in the body are ferritin, serum iron, total body mass and % transferrin saturation with iron.

Using indicators of iron metabolism in the body allows the clinician to:
- identify the presence and nature of iron metabolism disorders in the body;
- identify the presence of iron deficiency in the body at the preclinical stage;
- carry out differential diagnosis of hypochromic anemia;
- evaluate the effectiveness of the therapy.

Treatment of Iron Deficiency Anemia:

In all cases of iron deficiency anemia, it is necessary to establish the immediate cause of this condition and, if possible, eliminate it (most often, eliminate the source of blood loss or treat the underlying disease, complicated by sideropenia).

Treatment of iron deficiency anemia should be pathogenetically substantiated, comprehensive and aimed not only at eliminating anemia as a symptom, but also at eliminating iron deficiency and replenishing its reserves in the body.

Iron deficiency anemia treatment program:
- eliminating the cause of iron deficiency anemia;
- therapeutic nutrition;
- ferrotherapy;
- prevention of relapses.

Patients with iron deficiency anemia are recommended to have a varied diet, including meat products (veal, liver) and products of plant origin (beans, soy, parsley, peas, spinach, dried apricots, prunes, pomegranates, raisins, rice, buckwheat, bread). However, it is impossible to achieve an antianemic effect with diet alone. Even if the patient eats high-calorie foods containing animal protein, iron salts, vitamins, and microelements, iron absorption of no more than 3-5 mg per day can be achieved. The use of iron supplements is necessary. Currently, the doctor has at his disposal a large arsenal of iron medications, characterized by different compositions and properties, the amount of iron they contain, the presence of additional components that affect the pharmacokinetics of the drug, and various dosage forms.

According to the recommendations developed by WHO, when prescribing iron supplements, preference is given to drugs containing divalent iron. The daily dose should reach 2 mg/kg of elemental iron in adults. The total duration of treatment is at least three months (sometimes up to 4-6 months). An ideal iron-containing drug should have a minimum number of side effects, have a simple regimen of use, the best efficiency/price ratio, optimal iron content, and preferably the presence of factors that enhance absorption and stimulate hematopoiesis.

Indications for parenteral administration of iron preparations arise in case of intolerance to all oral drugs, malabsorption (ulcerative colitis, enteritis), gastric and duodenal ulcers during an exacerbation, with severe anemia and the vital need to quickly replenish iron deficiency. The effectiveness of iron supplements is judged by changes in laboratory parameters over time. By the 5-7th day of treatment, the number of reticulocytes increases by 1.5-2 times compared to the initial data. Starting from the 10th day of therapy, the hemoglobin content increases.

Considering the pro-oxidant and lysosomotropic effect of iron preparations, their parental administration can be combined with intravenous drip administration of rheopolyglucin (400 ml - once a week), which protects the cell and avoids iron overload of macrophages. Considering significant changes in the functional state of the erythrocyte membrane, activation of lipid peroxidation and a decrease in antioxidant protection of erythrocytes in iron deficiency anemia, it is necessary to introduce antioxidants, membrane stabilizers, cytoprotectors, antihypoxants into the treatment regimen, such as a-tocopherol up to 100-150 mg per day (or ascorutin, vitamin A, vitamin C, lipostabil, methionine, mildronate, etc.), and also combined with vitamins B1, B2, B6, B15, lipoic acid. In some cases, it is advisable to use ceruloplasmin.

List of drugs used in the treatment of iron deficiency anemia:

Hypochromic anemia includes several types of anemia in which red blood cells are poorly colored and therefore are not able to carry a sufficiently large amount of oxygenated hemoglobin. All types are included in the list of hypochromic anemia, ICD code 10. Microcytic anemia most often occurs due to the lack of adequate iron reserves in the blood. Treatment usually consists of replenishing iron stores.

Microcytic anemia is one of many types of anemia whose characteristic features include the appearance of an excess of red blood cells. They are small (medically called microcytes), this is a normocytic hypochromic anemia. The main blood count measure that shows us microcytic anemia is MCV (mean blood cell volume). If it is microcytic anemia, the MCV cutoff is 80 fL (or less).

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

Hypochromic anemia in children is divided into:

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

Hypochromic iron deficiency anemia

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

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

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

3 Poor nutrition(lack of consumption of foods rich in absorbable iron - red meat, eggs, liver, plants with green leaves - is often accompanied by an incorrect composition of the vegetarian diet).

4 Iron absorption disorders(many diseases limit the intestines' ability to absorb iron, such as celiac disease, inflammatory bowel and stomach diseases, and conditions following surgery to remove long sections of the small intestine).

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

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

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

Chronic hypochromic anemia

Diagnosis of microcytic anemia with iron deficiency should be supplemented by excluding other, equally important causes of this disease.

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

2 Sideroblastic anemia. This cause of microcytic anemia is poorly understood. It is known to create abnormal cells called sideroblasts. This may be a disorder that is congenital or occurs during life (caused by certain medications or other medical conditions). It is diagnosed by carefully analyzing the blood picture and searching for factors that cause its occurrence.

Symptoms of microcytic anemia

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

  • a feeling of fear and a sense of threat;
  • irritability;
  • chest pain;
  • constipation;
  • excessive sleepiness;
  • mouth ulcers;
  • noise in ears;
  • cardiopalmus;
  • hair loss;
  • loss of consciousness or a feeling of approaching unconsciousness;
  • depression;
  • apnea;
  • involuntary muscle cramps;
  • pale yellow skin;
  • nausea;
  • burning sensation in the abdomen;
  • menstrual disorders (no cycle);
  • inflammation or infection of the surface of the tongue;
  • inflammation of the corners of the mouth;
  • weakness of appetite;
  • difficulty swallowing;
  • insomnia;
  • restless legs syndrome.

Treatment of hypochromic anemia and prognosis

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

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


Anemia is a discrepancy between the proportion of hemoglobin in a person’s blood and the criteria adopted by the World Health Organization for a specific age and gender. The term "anemia" is not a diagnosis of the disease, but only indicates abnormal changes in the blood test.

Code according to the international classification of diseases ICD-10: iron deficiency anemia – D50.

The most common are anemia due to blood loss and iron deficiency anemia:

  1. Anemia due to blood loss can be caused by prolonged menstruation, bleeding in the digestive tract and urinary tract, injuries, surgeries, and cancer.
  2. Iron-deficiency anemia formed as a result of a deficiency in the body's production of red blood cells

Causes and factors

Among the factors that increase the risk of developing anemia, doctors identify:

  • insufficient intake of iron, vitamins and minerals;
  • poor nutrition;
  • blood loss due to injury or surgery;
  • kidney disease;
  • diabetes;
  • rheumatoid arthritis;
  • HIV AIDS;
  • inflammatory bowel diseases (including Crohn's disease);
  • liver diseases;
  • heart failure;
  • thyroid diseases;
  • anemia after illness caused by infection.

It is a misconception that anemia occurs only after illness.

There are many more reasons:


Degrees and types of anemia

  1. lungs– the amount of hemoglobin is 90 g/l and above;
  2. average degree of severity - hemoglobin 70-90 g/l;
  3. heavy anemia - hemoglobin below 70 g/l, with the norm for women being 120-140 g/l, for men - 130-160 g/l.
  • Anemia due to iron deficiency. Women during pregnancy, menstruation and lactation need several times more iron than usual. Therefore, iron deficiency anemia often occurs during this period.
    It's the same with a child's body. requires a lot of iron. This anemia can be treated with iron tablets or syrups.
  • Megaloblastic anemia occurs as a result of thyroid hormone deficiency, liver disease and tuberculosis. This type of anemia is caused by a lack of vitamin B12 and folic acid. Early diagnosis and treatment are very important for patients with megaloblastic anemia.
    Weakness, fatigue, numbness of the hands, pain and burning of the tongue, shortness of breath are common complaints of this type of disease.
  • Chronic infectious anemia occurs due to a lack of bone marrow, with tuberculosis, leukemia and as a result of taking certain medications that contain toxic substances.
  • Mediterranean anemia(disease also known as thalassemia) is an inherited blood disorder. A high incidence of this type is observed in Italians and Greeks. At the initial stage, the symptoms are the same as those of anemia due to iron deficiency.
    As the disease progresses jaundice is observed, anemia is added as a result of kidney disease and spleen growth. Thalassemia is treated with blood transfusions.
  • Sickle cell anemia This is also a hereditary disease in which the structure of hemoglobin in the blood differs from normal values. The red blood cell takes the shape of a crescent and its lifespan is very short. This type is observed in representatives of the black race. Women carry the gene for this anemia.
  • Aplastic anemia This is a disruption of the production of red blood cells in the bone marrow. The cause may be evaporation of harmful substances such as benzene, arsenic, and exposure to radiation. Blood cell platelet levels also decrease.
    The opposite of aplastic anemia is polycythemia, during which the normal number of red blood cells more than doubles. The patient's skin becomes red and there may be an increase in blood pressure. The reason for this is lack of oxygen. This disease is treated by removing blood from the human body.

Who can get anemia?

Anemia is a disease that affects all age groups, ethnic groups, and races.

  • Some children in the first year of life are at risk of anemia due to iron deficiency. These are premature births and children who were fed breast milk with a lack of iron. These infants develop anemia within the first 6 months.
  • Children aged one to two years are susceptible to developing anemia. Especially if they drink a lot of cow's milk and don't eat foods with enough iron. Cow's milk does not contain enough iron for a child's growth. Instead of milk A child under 3 years of age should be fed iron-rich foods. Cow's milk may also prevent the body from absorbing iron.
  • Researchers continue to study How does anemia affect adults? More than ten percent of adults are constantly mildly anemic. Most of these people have other medical diagnoses.

Signs and symptoms

The most common symptom of anemia is fatigue. People feel tired and exhausted.

Other signs and symptoms of anemia include:

  • difficulty breathing;
  • dizziness;
  • headache;
  • cold feet and palms;
  • chest pain.

These symptoms may occur because the heart has a harder time pumping oxygen-rich blood into the body.

In mild to moderate anemia (iron deficiency type), symptoms are:

  • desire to eat a foreign object: earth, ice, limestone, starch;
  • cracks in the corners of the mouth;
  • irritated tongue.

Signs of folic acid deficiency:

  • diarrhea;
  • depression;
  • swollen and red tongue;

Symptoms of anemia due to lack of vitamin B12:

  • tingling and loss of sensation in the upper and lower extremities;
  • difficulty distinguishing between yellow and blue colors;
  • swelling and pain in the larynx;
  • weight loss;
  • blackening of the skin;
  • diarrhea;
  • depression;
  • decreased intellectual function.

Complications

When announcing the diagnosis, the doctor must warn about the dangers of anemia:

  1. Patients may experience arrhythmia– a problem with the speed and rhythm of heart contractions. Arrhythmia can lead to heart damage and heart failure.
  2. Anemia may also cause damage to other organs in the body: the blood cannot supply the organs with enough oxygen.
  3. For cancer and HIV/AIDS disease can weaken the body and reduce the results of treatment.
  4. Increased risk the occurrence of anemia in kidney disease, in patients with heart problems.
  5. Some types of anemia occur when there is insufficient fluid intake or excessive loss of water in the body. Severe dehydration is a cause of blood disease.

Diagnostics

The doctor should obtain a family history of the disease to determine whether the disease is hereditary or acquired. He may ask the patient about general signs of anemia and whether he is on a diet.

Physical examination is:

  1. listening to heart rhythm and breathing regularity;
  2. measuring the size of the spleen;
  3. presence of pelvic or rectal bleeding.
  4. Laboratory tests will help determine the type of anemia:
    • general blood analysis;
    • hemograms.

The hemogram test measures the hemoglobin and hematocrit values ​​in the blood. Low hemoglobin and hematocrit are a sign of anemia. Normal values ​​vary by race and population.

Other tests and procedures:

  • Hemoglobin electrophoresis determines the amount of different types of hemoglobin in the blood.
  • Reticulocyte measurement is a count of young red blood cells in the blood. This test shows the rate of red blood cell production by the bone marrow.
  • Tests to measure iron in the blood– this is a determination of the level and total iron content, transmission, and binding capacity of the blood.
  • If the doctor suspects anemia due to blood loss, he may suggest a test to determine the source of the bleeding. He will suggest taking a stool test to determine blood in the stool.
    If there is blood, endoscopy is necessary: examination of the inside of the digestive system with a small camera.
  • May need also bone marrow analysis.

How is anemia treated?

Treatment for anemia depends on the cause, severity and type of illness. The goal of treatment is to increase oxygen in the blood by multiplying red cells and increasing hemoglobin levels.

Hemoglobin is a protein that transports oxygen to the body with the help of iron.

Changes and additions to the diet

Iron

The body needs iron to form hemoglobin. The body absorbs iron from meat more easily than from vegetables and other foods. To treat anemia, you need to eat more meat, especially red meat (beef or liver), as well as chicken, turkey and seafood.

In addition to meat, iron is found in:


Vitamin B12

Low levels of vitamin B12 can lead to pernicious anemia.

Sources of vitamin B12 are:

  • cereals;
  • red meat, liver, poultry, fish;
  • eggs and dairy products (milk, yogurt and cheese);
  • Iron-based soy drinks and vegetarian foods fortified with vitamin B12.

Folic acid

The body needs folic acid to produce new cells and protect them. Folic acid is essential for pregnant women. It protects against anemia and promotes healthy fetal development.

Good food sources of folic acid are:

  • bread, pasta, rice;
  • spinach, dark green leafy vegetables;
  • dry beans;
  • liver;
  • eggs;
  • bananas, oranges, orange juice and some other fruits and juices.

Vitamin C

It helps the body absorb iron. Fruits and vegetables, especially citrus fruits, are a good source of vitamin C. Fresh and frozen fruits and vegetables contain more vitamin C than canned foods.

Kiwis, strawberries, melons, broccoli, peppers, Brussels sprouts, tomatoes, potatoes, spinach, and radishes are rich in vitamin C.

Medicines

Your doctor may prescribe medications to treat the underlying cause of anemia and increase the number of red blood cells in your body.

It can be:

  • antibiotics to treat infections;
  • hormones to prevent excessive menstrual bleeding in young girls and women;
  • artificial erythropoietin to stimulate the production of red blood cells.

Operations

If anemia develops into a severe stage, surgery may be required: blood and bone marrow stem cell transplantation, blood transfusion.

Stem cell transplantation is carried out to replace damaged ones in a patient from another healthy donor. Stem cells are found in the bone marrow. The cells are transferred through a tube inserted into a vein in the chest. The process is similar to a blood transfusion.

Surgical interventions

For life-threatening bleeding in the body that causes anemia, surgical intervention is necessary.

For example, anemia due to stomach ulcers or colon cancer requires surgery to prevent bleeding.

Prevention

Some types of anemia can be prevented by eating foods rich in iron and vitamins. It is useful to take nutritional supplements while dieting.

Important! For women who are keen on losing weight and various diets, taking additional iron supplements and vitamin complexes is a must!

After basic treatment for anemia, you need to keep in touch with your doctor and regularly check your blood composition.

If the patient has inherited a pernicious type of anemia, treatment and prevention should last for years. You need to be prepared for this.

Anemia in children and youth

Chronic diseases, iron deficiency and poor nutrition can lead to anemia. The disease is often accompanied by other health problems. Thus, the signs and symptoms of anemia are often not so obvious.

You should definitely consult a doctor if you experience symptoms of anemia or if you are on a diet. You may need a blood transfusion or hormone therapy. If anemia is diagnosed early, it can be completely cured.

D50- D53- diet-related anemias:

D50 - iron deficiency;

D51 - vitamin B 12 – deficient;

D52 - folate deficiency;

D53 - other diet-related anemias.

D55- D59- hemolytic anemia:

D55- associated with enzymatic disorders;

D56 - thalassemia;

D57 - sickle cell;

D58 - other hereditary hemolytic anemias;

D59-acute acquired hemolytic.

D60- D64- aplastic and other anemias:

D60 - acquired red cell aplasia (erythroblastopenia);

D61-other aplastic anemia;

D62 - acute aplastic anemia;

D63-anemia of chronic diseases;

D64 - other anemias.

Pathogenesis

The supply of oxygen to tissues is provided by red blood cells - the formed elements of blood that do not contain a nucleus; the main volume of the red blood cell is occupied by hemoglobin - a protein that binds oxygen. The lifespan of red blood cells is about 100 days. When the hemoglobin concentration is below 100-120 g/l, oxygen delivery to the kidneys decreases, this stimulates the production of erythropoietin by the interstitial cells of the kidneys, which leads to the proliferation of erythroid cells of the bone marrow. For normal erythropoiesis it is necessary:

    healthy bone marrow

    healthy kidneys that produce enough erythropoietin

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

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

Figure 1. Scheme of red blood cell formation. (T.R. Harrison).

Clinical picture

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

When the Hb concentration is below 70-80 g/l, fatigue, shortness of breath during exercise, palpitations, and throbbing headaches appear.

In elderly patients with cardiovascular diseases, there is an increase in pain in the heart and an increase in signs of heart failure.

Acute blood loss leads to a rapid decrease in the number of red blood cells and blood volume. It is necessary, first of all, to assess the state of hemodynamics. Redistribution of blood flow and venous spasm cannot compensate for acute blood loss of more than 30%. Such patients lie down and have severe orthostatic hypotension and tachycardia. Loss of more than 40% of blood (2000 ml) leads to shock, the signs of which are tachypnea and tachycardia at rest, stupor, cold sticky sweat, and decreased blood pressure. Emergency restoration of the central circulation is necessary.

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

Paleness of the skin and mucous membranes becomes noticeable when the Hb concentration decreases to 80-100 g/l. Jaundice can also be a sign of anemia. When examining a patient, attention is paid to the condition of the lymphatic system, the size of the spleen and liver is determined, ossalgia is detected (pain when pounding bones, especially the sternum), attention should be drawn to petechiae, ecchymoses and other signs of coagulation disorders or bleeding.

Severity of anemia(by Hb level):

    slight decrease in Hb 90-120 g/l

    average Hb 70-90 g/l

    heavy Hb<70 г/л

    extremely heavy Hb<40 г/л

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

    Are there any signs of bleeding or has it already occurred?

    Are there signs of excessive hemolysis?

    Are there signs of suppression of bone marrow hematopoiesis?

    Are there any signs of iron metabolism disorders?

    Are there signs of vitamin B12 or folic acid deficiency?

Treatment of IDA includes treatment of the pathology that led to iron deficiency and the use of iron-containing drugs to restore iron reserves in the body. Identification and correction of pathological conditions that cause iron deficiency are the most important elements of complex treatment. Routine administration of iron-containing drugs to all patients with IDA is unacceptable, since it is not effective enough, is expensive and, more importantly, is often accompanied by diagnostic errors (non-detection of neoplasms).
The diet of patients with IDA should include meat products containing heme iron, which is absorbed better than from other products. It must be remembered that severe iron deficiency cannot be compensated for by diet alone.
Treatment of iron deficiency is carried out mainly with oral iron-containing drugs; parenteral drugs are used if there are special indications. It should be noted that the use of iron-containing oral medications is effective in most patients, whose body is able to absorb a sufficient amount of pharmacological iron to correct the deficiency. Currently, a large number of drugs containing iron salts are produced (ferroplex, orferon, tardiferon). The most convenient and cheapest are preparations containing 200 mg of ferrous sulfate, i.e. 50 mg of elemental iron in one tablet (ferrocal, ferroplex). The usual dose for adults is 1-2 tablets. 3 times a day. An adult patient should receive at least 3 mg of elemental iron per kg of body weight per day, i.e. 200 mg per day. The usual dosage for children is 2-3 mg of elemental iron per kg of body weight per day.
The effectiveness of preparations containing ferrous lactate, succinate or fumarate does not exceed the effectiveness of tablets containing ferrous sulfate or gluconate. The combination of iron salts and vitamins in one preparation, with the exception of the combination of iron and folic acid during pregnancy, as a rule, does not increase iron absorption. Although this effect can be achieved with large doses of ascorbic acid, the resulting adverse effects make therapeutic use of such a combination inappropriate. The effectiveness of slow-acting (retard) drugs is usually lower than that of conventional drugs because they enter the lower intestine, where iron is not absorbed, but it may be higher than that of fast-acting drugs taken with food.
It is not recommended to take a break of less than 6 hours between taking tablets, since for several hours after using the drug, duodenal enterocytes are refractory to iron absorption. Maximum absorption of iron occurs when taking the tablets on an empty stomach; taking it during or after meals reduces it by 50-60%. Do not take iron-containing medications with tea or coffee, which inhibit iron absorption.
Most adverse events when using iron-containing drugs are associated with gastrointestinal irritation. In this case, adverse events associated with irritation of the lower gastrointestinal tract (moderate constipation, diarrhea) usually do not depend on the dose of the drug, while the severity of irritation of the upper gastrointestinal tract (nausea, discomfort, pain in the epigastric region) is determined by the dose. Adverse effects are less common in children, although in them the use of iron-containing liquid mixtures may lead to temporary darkening of the teeth. To avoid this, you should give the drug to the root of the tongue, take the medicine with liquid and brush your teeth more often.
If there are severe side effects associated with irritation of the upper gastrointestinal tract, you can take the drug after meals or reduce the single dose. If adverse effects persist, you can prescribe drugs containing smaller amounts of iron, for example, in the composition of ferrous gluconate (37 mg of elemental iron per tablet). If in this case the adverse events do not stop, then you should switch to slow-acting drugs.
Improvement in the well-being of patients usually begins on the 4-6th day of adequate therapy, on the 10-11th day the number of reticulocytes increases, on the 16th-18th day the hemoglobin concentration begins to increase, microcytosis and hypochromia gradually disappear. The average rate of increase in hemoglobin concentration with adequate therapy is 20 g/l over 3 weeks. After 1-1.5 months of successful treatment with iron supplements, the dose can be reduced.
The main reasons for the lack of the expected effect when using iron-containing drugs are presented below. It should be emphasized that the main reason for the ineffectiveness of such treatment is ongoing bleeding, therefore identifying the source and stopping the bleeding is the key to successful therapy.
The main reasons for the ineffectiveness of treatment for iron deficiency anemia: ongoing blood loss; inappropriate use of medications:
- incorrect diagnosis (anemia in chronic diseases, thalassemia, sideroblastic anemia);
- combined deficiency (iron and vitamin B12 or folic acid);
- taking slow-acting medications containing iron: impaired absorption of iron supplements (rare).
It is important to remember that in order to restore iron reserves in the body in case of severe deficiency, the duration of taking iron-containing drugs should be at least 4-6 months or at least 3 months after normalization of hemoglobin levels in peripheral blood. The use of oral iron supplements does not lead to iron overload, since absorption is sharply reduced when iron stores are restored.
Prophylactic use of oral iron-containing drugs is indicated during pregnancy, patients receiving chronic hemodialysis, and blood donors. For premature babies, the use of nutritional mixtures containing iron salts is recommended.
Patients with IDA rarely need the use of parenteral drugs containing iron (ferrum-lek, imferon, ferkoven, etc.), since they usually respond quickly to treatment with oral drugs. Moreover, adequate therapy with oral medications, as a rule, is well tolerated even by patients with gastrointestinal pathology (peptic ulcer, enterocolitis, ulcerative colitis). The main indications for their use are the need to quickly compensate for iron deficiency (significant blood loss, upcoming surgery, etc.), severe side effects of oral medications, or impaired iron absorption due to damage to the small intestine. Parenteral administration of iron supplements may be accompanied by severe side effects and may also lead to excessive accumulation of iron in the body. Parenteral iron preparations do not differ from oral preparations in the rate of normalization of hematological parameters, although the rate of restoration of iron reserves in the body when using parenteral preparations is much higher. In any case, the use of parenteral iron supplements can be recommended only if the doctor is convinced that treatment with oral medications is ineffective or intolerable.
Iron preparations for parenteral use are usually administered intravenously or intramuscularly, with the intravenous route of administration being preferred. They contain from 20 to 50 mg of elemental iron per ml. The total dose of the drug is calculated using the formula:
Iron dose (mg) = (Hemoglobin deficiency (g/l)) / 1000 (Circulating blood volume) x 3.4.
The volume of circulating blood in adults is approximately 7% of body weight. To restore iron stores, 500 mg is usually added to the calculated dose. Before starting therapy, 0.5 ml of the drug is administered to exclude an anaphylactic reaction. If there are no signs of anaphylaxis within 1 hour, then the drug is administered so that the total dose is 100 mg. After this, 100 mg is administered daily until the total dose of the drug is reached. All injections are given slowly (1 ml per minute).
An alternative method involves simultaneous intravenous administration of the entire total dose of iron. The drug is dissolved in 0.9% sodium chloride solution so that its concentration is less than 5%. The infusion is started at a rate of 10 drops per minute; if there are no adverse events within 10 minutes, the rate of administration is increased so that the total duration of the infusion is 4-6 hours.
The most severe side effect of parenteral iron supplements is an anaphylactic reaction, which can occur with both intravenous and intramuscular administration. Although such reactions occur relatively rarely, the use of parenteral iron supplements should only be carried out in medical institutions that are fully equipped to provide emergency care. Other undesirable effects include facial flushing, increased body temperature, urticarial rash, arthralgia and myalgia, phlebitis (if the drug is administered too quickly). Drugs should not get under the skin. The use of parenteral iron supplements can lead to activation of rheumatoid arthritis.
Red blood cell transfusions are performed only in cases of severe IDA, accompanied by severe signs of circulatory failure, or upcoming surgical treatment.