Symptoms and treatment of anemia. Iron deficiency anemia Chronic iron deficiency anemia ICD code 10

Differential diagnosis of anemic syndromes is an important detail in patient management, since treatment approaches will differ depending on the pathogenesis.

Therefore, iron deficiency anemia according to ICD 10 has the code D50, which distinguishes it from other types of this syndrome.

Some chronic IDA are pathologies associated with intense blood loss, that is, appearing as a result hemorrhagic syndrome, and IDA of primary origin. The mechanism for the development of hypochromic anemia without blood loss is associated with a lack of iron intake into the body, with immune processes that block its transformation or pathologies that cause malabsorption.

Hypochromic anemia is always accompanied by a lack of hemoglobin in red blood cells, which contains iron.

Features of ZhDA

Anemic syndrome does not give specific manifestations, therefore the mechanism of its development: lack of elements, hematopoietic problems, pronounced breakdown of red blood cells - are determined in the laboratory. In ICD 10 iron deficiency anemia is coded D50, which assumes the following diagnostic criteria:

• decrease in the number of red blood cells;
• decline color index;
• decrease in the amount of hemoglobin;
• low serum iron level (with refractory anemia, the level, on the contrary, increases significantly).

Medical institutions use individual treatment protocols of this disease. However, the ZDA code implies general principles therapy, the basis of which is iron supplements.

U healthy person all basic blood values ​​​​should be normal, any deviation is a sign of development pathological processes. Anemia is characterized by a decrease in the number of red blood cells and low hemoglobin; the causes of the disease are congenital or acquired; often the disease occurs due to poor nutrition.

Due to the reduction of red cells, anemia is called anemia

Anemia - what is it?

– a disease that is manifested by a significant decrease in hemoglobin and the number of red blood cells. The disease code according to ICD-10 is D50–D89.

Anemia is not the main disease; the pathology always develops against the background of work failures internal organs and systems.

Classification of anemia

Since there are many reasons for the development of anemia, they manifest themselves with different symptoms, each form requires special drug therapy, and the disease is classified according to certain indicators.

In any form of anemia, hemoglobin values ​​are always below acceptable limits, and the number of red blood cells may be normal or decreased.

By color index

Color index– level of saturation of red blood cells with hemoglobin. To calculate the erythrocyte hemoglobin index, multiply by 3 and divide by the whole number of red blood cells.

Classification:

With normochromic anemia, indicators only sometimes go beyond acceptable limits

• hypochromic– color index up to 0.8 units;
• normochromic– color index 0.6–1.05 units;
• hyperchromic– the color index value exceeds 1.05 units.

The diameter of red blood cells is 7.2–8 microns. An increase in size is a sign of a deficiency of vitamin B-9, B-12, a decrease indicates a lack of iron.

According to the ability of bone marrow to regenerate

The process of creating new cells occurs in the tissues of the main organ of the hematopoietic system, the main indicator of the normal functioning of the body is the presence in the blood of the required number of reticulocytes, primary red cells, the rate of their formation is called erythropoiesis.

Classification:

• regenerative – the number of reticulocytes is 0.5–2%, the regeneration rate is normal;
• hyporegenerative – there is a decrease in regenerative functions, the number of reticulocytes is 0.5%;
• hyperregenerative – accelerated process tissue repair bone marrow, reticulocytes in the blood more than 2%;
• aplastic - there are no reticulocytes, or their value does not exceed 0.2%.

It takes 2–3 hours to synthesize new red blood cells.

According to the mechanism of pathology development

Anemia occurs as a result of severe blood loss, disruption of the formation of red blood cells or their rapid disruption; according to the mechanism of development, the disease is divided into several categories.

Kinds:

• anemia due to severe blood loss, chronic bleeding;
• iron deficiency, renal, B12 and folic form, aplastic - these types of disease arise due to problems in the process of hematopoiesis;
• with some autoimmune disorders, against the background of poor heredity, red blood cells are intensively destroyed, anemia develops.

Short-term mild anemia occurs in women during menstruation, after childbirth. If there are no serious abnormalities in the body, to improve well-being it is enough to adjust the diet and normalize the daily routine.

Severity of anemia

There are 3 degrees of severity of the pathological condition, depending on how much the actual hemoglobin values ​​are below the permissible norm.

Hemoglobin norms

Before classifying anemia, test for hemoglobin levels

Severity:

• 1st degree – hemoglobin within 90 g/l;
• 2nd degree – hemoglobin 70–90 g/l;
• Grade 3 – hemoglobin 70 g/l or less.

Mild forms of the disease are characterized by a slight deterioration of the condition; severe anemia poses a serious threat to the health of adults; for a child, pathological changes can be fatal.

Symptoms and clinical manifestations

With anemia, gas exchange is disrupted; against the background of a decrease in the number of red blood cells, they transport carbon dioxide and oxygen worse. Some of the main signs of any type of disease anemic syndrome– attacks of dizziness, drowsiness, increased fatigue, irritability, pale skin, headaches. Photos of sick people will allow you to determine the external signs of the disease.

Anemia due to erosive gastritis

Anemia causes pale skin

Type of anemia	Symptoms and external manifestations
Iron deficiency	Concentration problems, shortness of breath, disturbance heart rate, convulsions, with internal bleeding, the stool becomes black. External signs– jams, white spots on the surface of the nail plates, the skin flakes, the hair loses its shine, splits, the surface of the tongue is glossy.
B12 deficient	Noise in the ears, flashing black spots, cardiopalmus, hypertension, tachycardia, shortness of breath, constipation. External signs are skin with a yellow tint, a scarlet, shiny tongue, multiple ulcers in the mouth, weight loss. The disease is accompanied by numbness, weakness in the limbs, cramps, and muscle atrophy.
Folate deficiency	Chronic fatigue, sweating, rapid heartbeat, pale skin, rarely an enlarged spleen.
Aplastic or hypoplastic anemia	Frequent migraine attacks, shortness of breath, fatigue, swelling lower limbs, increased susceptibility to infectious diseases, causeless fever. External manifestations– bleeding gums, ulcers in the mouth, small red rash, the appearance of bruises even after minor blows, a jaundiced tint of the skin.
Hemolytic	Tachycardia, hypotension, rapid breathing, nausea, abdominal pain, constipation or diarrhea, urine becomes dark in color. External signs are pallor, jaundice, hyperpigmentation of the skin, deterioration of the nails, ulcers on the lower extremities.
Posthemorrhagic	Severe weakness, frequent attacks of dizziness, vomiting, shortness of breath, cold sweat, thirst, decreased temperature and blood pressure, increased heart rate. External signs are poor condition of hair and nail plates, unhealthy skin color.
sickle cell	Intolerance to stuffy rooms, jaundice, vision problems, discomfort in the spleen area, ulcerative skin lesions appear on the legs.

With a lack of iron, strange taste preferences appear - a person wants to eat lime, raw meat. Olfactory perversions are also observed - patients like the smell of dyes and gasoline.

Causes of anemia

Anemia is a consequence of massive or prolonged bleeding, a decrease in the rate of appearance of new red blood cells, and the rapid destruction of red blood cells. The disease often indicates a chronic or acute deficiency of iron, folic and ascorbic acid, vitamin B12, with excessive adherence to strict diets and fasting.

Type of anemia	Changes in blood parameters	Causes
Iron deficiency	Low values ​​of color index, red blood cells, iron and hemoglobin levels.	· vegetarianism, poor diet, constant diets; · gastritis, ulcers, gastric resections; · pregnancy, period of natural feeding, puberty; · chronic bronchitis, heart disease, sepsis, abscess; · pulmonary, renal, uterine, gastrointestinal, bleeding.
B12-deficient	A type of hypochromic anemia, increased reticulocyte content.	· chronic lack of vitamin B 9, B12; · atrophic form gastritis, resection, malignant neoplasms of the stomach; · infection with worms, intestinal infectious diseases; · multiple pregnancy, physical fatigue; · cirrhosis of the liver.
Folate deficiency	A type of hyperchromic anemia, low vitamin B9.	Lack of products with vitamin B9 in the menu, cirrhosis, alcohol poisoning, celiac disease, pregnancy, the presence of malignant neoplasms.
Aplastic	Decrease in leukocytes, erythrocytes, platelets.	· changes in stem cells, disturbances in the process of hematopoiesis, poor absorption of iron and vitamin B12; · hereditary pathologies; · long-term use of NSAIDs, antibiotics, cytostatics; · poisoning with toxic substances; · parvovirus infection, immunodeficiency states; · autoimmune problems.
Hemolytic	Red blood cells are quickly destroyed, the number of old red blood cells significantly exceeds the number of new ones. The hemoglobin level and the number of red blood cells are below acceptable limits.	· defects of erythrocytes, disturbances in the structure of hemoglobin; · poisoning by poisons, long-term use of antiviral and antibacterial medications; · malaria, syphilis, viral pathologies; · defects of artificial heart valve; thrombocytopenia.
Sickle cell is a subtype of hemolytic anemia	A decrease in hemoglobin to 80 g/l, a decrease in red blood cells, an increase in the number of reticulocytes.	Hereditary pathology, hemoglobin molecules have a defect, they gather into twisted crystals, stretching the red blood cells. Damaged red blood cells have low plasticity, make the blood more viscous, and injure each other.
Posthemorrhagic	The number of leukocytes decreases, the content of reticulocytes and platelets increases.	Copious blood loss from wounds, uterine bleeding. Chronic blood loss - ulcerative lesions of the gastrointestinal tract, cancer of the stomach, liver, lungs, intestines, uterine fibroids, roundworm infection, poor clotting.

Stomach ulcers can cause chronic blood loss

Pseudoanemia is a decrease in blood viscosity with the disappearance of edema due to excessive fluid intake. Hidden anemia - thickening of the blood, occurs with excessive vomiting, diarrhea, excessive sweating, hemoglobin and red blood cells do not decrease.

Sometimes a person is diagnosed with mixed anemia, a decrease in hemoglobin of unknown origin, when it is not possible to identify the exact or sole cause of the pathology even after a thorough examination.

A decrease in hemoglobin in children is often congenital, secondary anemia– a consequence of unbalanced nutrition, active growth during puberty.

Thalassemia – severe hereditary disease, occurs due to an increase in the rate of hemoglobin formation, red blood cells have the shape of a target. Signs: jaundice, earthy-green tint of the skin, irregular shape of the skull and abnormal structure of bone tissue, mental abnormalities, physical development, the eyes have a Mongoloid section, the liver and spleen are enlarged.

The main signs of anemia are yellowness and whiteness.

Hemolytic anemia of newborns– occurs due to Rh conflict; at birth, the child is diagnosed with severe edema, ascites, and there are many immature red blood cells in the blood. The degree of pathology is determined based on hemoglobin and indirect bilirubin levels.

Spherocytic is a hereditary gene pathology in which red blood cells have a rounded shape and are quickly destroyed in the spleen. The consequence is the formation of stones in gallbladder, jaundice, irritability, nervousness.

Which doctor should I contact?

If anemia occurs, it is necessary to start. After receiving the results of the initial diagnosis further treatment will deal with , . If internal bleeding or tumors are suspected, urgent hospitalization is required.

Diagnostics

Main type of diagnosis– a detailed and complete blood test, using a hematological analyzer to determine the number of red blood cells, their structural features, color index values, hemoglobin, and to recognize inflammatory processes.

To identify pathology, take a full range of blood tests

Diagnostic methods:

• blood biochemistry;
• urine test to detect hemoglobin;
• stool examination for the presence hidden blood, worm eggs;
• fibrogastroduodenoscopy, colonoscopy – assessment of the condition of the stomach and other gastrointestinal organs;
• myelogram;
• Ultrasound of the organs of the reproductive, digestive, respiratory systems;
• CT scan of lungs, kidneys;
• fluorography;
• ECG, echocardiography;

Red blood cells live on average 90–120 days, and decay (hemolysis) occurs inside the blood vessels, in the bone marrow, liver and spleen. Any disruptions in the functioning of these organs provoke the occurrence of anemia.

Treatment of anemia

To raise hemoglobin, drugs are used in tablet form, in the form of injection solutions, droppers, which eliminate the main cause of anemia and enhance the effect of drugs - traditional methods.

When internal bleeding is diagnosed, surgery is performed; in severe cases, blood transfusion or purification, bone marrow transplantation, and removal of the spleen are required.

Medicines

Medicines are selected based on test results, the type and severity of anemia, and the main diagnosis.

How to treat:

Aktiferrin – iron-replenishing drug

• Aktiferrin, Ferlatum – iron preparations, prescribed in combination with vitamin C;
• intramuscular injection of vitamin B12;
• medications with folic acid;
• immunosuppressants, antimetabolites – Metojekt, Ecoral;
• glucocorticosteroids – Prednisol, Medopred;
• various types of immunoglobulins;
• means for accelerating the process of formation of red blood cells in stem cells - Epotal, Vepox.

In case of severe blood loss, measures are taken to replenish the volume of circulating blood - red blood cells, a solution of Albumin, Polyglucin, Gelatinol, and glucose are administered using droppers.

Folk remedies

Alternative medicine methods normalize the values ​​of basic blood parameters in mild forms of anemia; in severe, chronic types of the disease they are used only as a complementary therapy after preliminary consultation with your doctor.

Simple recipes:

1. Mix juice in equal proportions black radish, carrots, beets, simmer the mixture in the oven on low heat for 3 hours. Dosage for adults – 15 ml, for children – 5 ml, take the medicine three times a day.
2. Grind 100 g of fresh wormwood, pour in 1 liter of vodka, put in a dark place for 21 days. Take 5 drops before each meal.
3. To 200 ml of pomegranate juice add 100 ml of carrot, apple and lemon juice, 70 ml liquid honey. Place the mixture in the refrigerator for 48 hours. Drink 30 ml three times a day.
4. Grind 300 g of peeled garlic, pour in 1 liter of vodka, put in a dark place for 3 weeks. Drink 5 ml before meals.
5. Mix 175 ml of aloe juice, 75 ml of honey and 450 ml of Cahors, shake, put in the refrigerator. Drink 30 ml three times a day before meals.

The simplest method for eliminating and preventing anemia is to regularly consume an infusion of rose hips, 1 tbsp. l. of crushed raw materials, brew 1 liter of boiling water, leave for 8 hours in a thermos, or a well-wrapped pan.

For mild forms of anemia, consume 2 kg of watermelon per season, unless there are contraindications.

Possible consequences and complications

Without proper and timely therapy against the background of anemia, it weakens significantly. the immune system, the risk of developing severe viral and bacterial pathologies increases.

Why is anemia dangerous?

• pulmonary, renal and heart failure;
• neurological diseases;
• deterioration of memory, concentration;
• deformation of the skin, mucous membranes;
• deviations in mental and physical development in children;
• chronic diseases of the eyes, digestive and respiratory systems.

One of the consequences of anemia is memory impairment

In severe forms of anemia, tissue hypoxia develops, which can cause hemorrhagic and cardiogenic shock, hypotension, coma, death.

Features of anemia during pregnancy

All pregnant women are at risk; anemia is often diagnosed during this period, but hemoglobin levels and the number of red blood cells usually decrease slightly, and the general condition is normal. Causes– an increase in the liquid component of blood against the background of a decrease in the volume of blood cells.

Sometimes in the background frequent vomiting with toxicosis, with problems with iron absorption, true iron deficiency anemia occurs; pathology is observed when carrying two or more children, with frequent pregnancies.

Symptoms– fatigue, weakness, insomnia or drowsiness, severe shortness of breath, nausea, tendency to faint. The skin becomes dry and pale, nails break, and hair falls out greatly. This condition can cause miscarriage, gestosis, premature delivery, and childbirth is usually difficult. In pregnant women, the lower limit of hemoglobin level is 110 mg/l.

Basis of therapy– diet, the menu should contain more offal, dietary meat, fish, 15–35 mg of iron should be consumed per day, depending on the stage of pregnancy. Additionally, medications with ascorbic and folic acid, iron sulfate and hydroxide are prescribed.

If a woman is diagnosed with anemia during pregnancy, iron deficiency is often observed in the child in the first year of life.

Prevention

Proper, balanced diet– reduce the consumption of animal fats, replace them with vegetable ones, avoid low-carbohydrate diets, consume more honey, buckwheat and oatmeal, vegetables, fruits, berries.

Regular exercise will replenish your blood and prevent almost any disease

All types of liver, beef tongue, beef and poultry, fish, peas, buckwheat, beets, cherries and apples - all these products are rich in iron and maintain hemoglobin levels at the proper level.

– a common disease, it occurs 10 times more often in women than in men. Modern medicines and folk recipes will effectively help cope with pathology, avoid complications, and compliance with simple preventive measures will reduce the risk of developing the disease.

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. Detection and correction pathological conditions, which are the cause of iron deficiency, - essential elements 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 is 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 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 it impractical therapeutic use such a combination. The effectiveness of slow-acting (retard) drugs is usually lower than that of conventional drugs, since they enter the lower intestine, where iron is not absorbed, but it may be higher than that of fast-acting drugs. active 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. At the same time, adverse events associated with irritation of the lower gastrointestinal tract (moderate constipation, diarrhea) usually do not depend on the dose of the drug, while the severity of irritation of the upper 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 adverse events associated with irritation of the upper gastrointestinal tract, you can take the drug after meals or reduce 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 main reason the ineffectiveness of such treatment is ongoing bleeding, so identifying the source and stopping the bleeding is the key 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 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).
Alternative method consists in one-step intravenous administration 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 total duration infusion was 4-6 hours.
The most severe side effect of parenteral iron supplements is anaphylactic reaction, which can occur both with intravenous and intramuscular injection. 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 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.

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

Reasons 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.
  Exactly the same baby 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 prematurely born and children who were fed breast milk with iron deficiency. 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

Most common symptom 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. At oncological diseases 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 can ask the patient about common features anemia, 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 the determination of the level and general content iron, transmission, blood binding ability.
• 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 inside digestive system with a small chamber.
• 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 source food products 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

At life-threatening bleeding in the body causing anemia requires surgical intervention.

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 supplements with iron 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.

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, nutritional and metabolic disorders (E00-E90), human immunodeficiency virus [HIV] disease (B20-B24), injury, poisoning and certain other effects of exposure external reasons(S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)

This class contains the following blocks:

D50-D53 Anemia associated with nutrition

D55-D59 Hemolytic anemias

D60-D64 Aplastic and other anemias

D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions

D70-D77 Other diseases of the blood and hematopoietic organs

D80-D89 Selected disorders involving 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 external cause code (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)

Excluded: factor VIII deficiency c vascular disorder(D68.0)

D67 Hereditary factor IX deficiency

Factor IX (with functional impairment)

Thromboplastic plasma component

D68 Other bleeding disorders

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

Pregnancy, childbirth and postpartum period(O45.0, O46.0, O67.0, O72.3)

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

Excludes: hereditary capillary fragility (D69.8)

factor VIII deficiency:

With functional impairment (D66)

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

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

Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease

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

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

D68.4 Acquired coagulation factor deficiency.

Coagulation factor deficiency due to:

Vitamin K deficiency

Excludes: vitamin K deficiency in the newborn (P53)

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

D68.9 Coagulation disorder, unspecified

D69 Purpura and other hemorrhagic conditions

Excludes: benign hypergammaglobulinemic purpura (D89.0)

cryoglobulinemic purpura (D89.1)

idiopathic (hemorrhagic) thrombocythemia (D47.3)

lightning purple (D65)

thrombotic thrombocytopenic purpura (M31.1)

D69.0 Allergic purpura.

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

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

Excludes: von Willebrand disease (D68.0)

D69.2 Other non-thrombocytopenic purpura.

D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome

D69.4 Other primary thrombocytopenias.

Excluded: thrombocytopenia with absence radius(Q87.2)

transient neonatal thrombocytopenia (P61.0)

Wiskott-Aldrich syndrome (D82.0)

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

D69.6 Thrombocytopenia, unspecified

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

D69.9 Hemorrhagic condition, unspecified

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

D70 Agranulocytosis

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

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

Excludes: transient neonatal neutropenia (P61.5)

D71 Functional disorders of polymorphonuclear neutrophils

Receptor complex defect cell membrane. Chronic (children's) granulomatosis. Congenital dysphagocytosis

Progressive septic granulomatosis

D72 Other white blood cell disorders

Excludes: basophilia (D75.8)

immune disorders (D80-D89)

preleukemia (syndrome) (D46.9)

D72.0 Genetic abnormalities of leukocytes.

Anomaly (granulation) (granulocyte) or syndrome:

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

Excluded: increase lymph nodes(R59.-)

hypergammaglobulinemia NOS (D89.2)

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

Excludes: hereditary ovalocytosis (D58.1)

D75.1 Secondary polycythemia.

Decreased plasma volume

D75.2 Essential thrombocytosis.

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

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

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

D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system

Excludes: Letterer-Sieve disease (C96.0)

malignant histiocytosis (C96.1)

reticuloendotheliosis or reticulosis:

Histiocytic medullary (C96.1)

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

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

D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.

Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS

D76.2 Hemophagocytic syndrome associated with infection.

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

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

Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma

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

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

SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)

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

caused by human immunodeficiency virus [HIV] sarcoidosis

Excluded: autoimmune diseases(system) ODU (M35.9)

functional disorders of polymorphonuclear neutrophils (D71)

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

D80 Immunodeficiencies with predominant antibody deficiency

D80.0 Hereditary hypogammaglobulinemia.

Autosomal recessive agammaglobulinemia (Swiss type).

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

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

D80.2 Electoral deficit immunoglobulin A

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 content B cells

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 regulatory document to take into account morbidity, reasons for the population’s visits to medical institutions all departments, 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 caesarean section, early placental abruption, placental previa, 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 drugs.
• 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

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

• The reflex phase, which develops on the first day after blood loss. Redistribution and centralization of blood circulation begins, increases peripheral resistance vessels. In this case, there is a decrease in the number of red blood cells with normal values hemoglobin and hematocrit concentrations.
• 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 clinical analysis blood. 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 severe dryness in the 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 activities must be carried out very quickly, since quick loss 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 eliminate it. Even the loss of 10 - 15 ml of blood per day deprives the body of the entire amount of iron that was received during that day with food.

Held comprehensive examination patient, 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 it 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 are indicated to stimulate hematopoietic processes. medicines with iron. 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, fermented milk 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 form 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.