Anemia is one of the most common blood diseases among both adults and children.
To complete the medical documentation of a patient with anemia of any etiology, the doctor uses the anemia code according to ICD 10. There are different forms of the disease depending on the cause that led to a decrease in hemoglobin and red blood cells in the blood. Anemia can be iron deficiency, folate deficiency, B-12 deficiency, hemolytic, aplastic and unspecified.
Causes, clinical picture and treatment of the pathological condition
The general mechanism of development for any type of disease is a disruption in the functioning of the hematopoietic organs due to a chronic lack of certain nutrients or, in some cases, due to the rapid destruction of blood cells in the bloodstream. Immune disorders and exposure to toxic substances also play an important role.
In ICD 10, anemia is classified as a blood disease and has code D50-D64.
The main clinical symptoms are:
- weakness;
- pallor;
- dizziness;
- pathological changes in taste;
- pathological changes in the skin;
- headache;
- digestive problems;
- intoxication (with hemolytic forms).
Treatment is carried out depending on the cause of the pathological decrease in hemoglobin and red blood cells. It is imperative to choose the right diet and regimen for the patient. Unspecified anemia requires an extended comprehensive examination of the patient’s body and symptomatic treatment in the initial stages.
Chapter 2. ANEMIA
Chapter 2. ANEMIA
Anemia(from Greek haima - anemia) - This is a clinical and hematological syndrome characterized by a decrease in the hemoglobin content per unit volume of blood, often with a simultaneous decrease in the number of red blood cells and a change in their qualitative composition, which leads to a decrease in the respiratory function of the blood and the development of oxygen starvation of tissues, most often expressed by symptoms such as pallor of the skin, increased fatigue, weakness, headaches, dizziness, palpitations, shortness of breath, etc.
Anemia itself is not a disease, but is often included in the structure of a large number of independent diseases.
According to the mechanism of development, anemia is divided into three different groups
Anemia may occur as a result of blood loss due to bleeding or hemorrhage - posthemorrhagic anemia.
Anemia may be the result of an excess of the rate of destruction of red blood cells over their production - hemolytic anemia.
Anemia may result from insufficient or impaired production of red blood cells in the bone marrow - hypoplastic anemia.
Anemia is a decrease in hemoglobin content per unit volume of blood (<100 г/л), чаще при одновременном уменьшении количества (<4,0х10 12 /л) или общего объема эритроцитов. Заболеваемость анемией в 2001 г. составила 157 на 100 000 населения.
Classification criteria
Depending on the average erythrocyte volume there are:
Microcytic [mean erythrocyte volume (MEV) less than 80 fL (µm)];
Normocytic (SER - 81-94 fl);
Macrocytic anemia (SER >95 fL).
Based on the hemoglobin content in red blood cells, there are:
Hypochromic [average hemoglobin content in erythrocytes (ASHE) less than 27 pg];
Normochromic (SSGE - 27-33 pg);
Hyperchromic (SSGE - more than 33 pg) anemia.
Pathogenetic classification
1.Anemia due to blood loss.
Acute posthemorrhagic anemia.
Chronic posthemorrhagic anemia.
2. Anemia due to disorders of hemoglobin synthesis and iron metabolism.
Microcytic anemias:
Iron-deficiency anemia;
Anemia due to impaired iron transport (atransferritinemia);
Anemia due to impaired iron utilization (sideroblastic anemia);
Anemia due to impaired iron recycling (anemia in chronic diseases).
Normochromic-normocytic anemia:
Hyperproliferative anemia (with kidney disease, hypothyroidism, protein deficiency);
Anemia caused by bone marrow failure (aplastic anemia, refractory anemia in myelodysplastic syndrome);
Metaplastic anemia (with hemoblastosis, metastases in the red bone marrow);
Dyserythropoietic anemia.
Macrocytic anemias:
Vitamin B12 deficiency;
Folic acid deficiency;
Copper deficiency;
Vitamin C deficiency.
3. Hemolytic anemia.
Purchased:
Hemolytic anemia caused by immune disorders [isoimmune hemolytic anemia, autoimmune hemolytic anemia (with warm or cold antibodies), paroxysmal nocturnal hemoglobinuria];
Hemolytic microangiopathic anemia;
Hereditary:
Hemolytic anemia associated with a violation of the structure of the erythrocyte membrane (hereditary spherocytosis, hereditary elliptocytosis);
Hemolytic anemia associated with enzyme deficiency in erythrocytes (glucose-6-phosphate dehydrogenase deficiency, pyruvate kinase deficiency);
Hemolytic anemia associated with impaired Hb synthesis (sickle cell anemia, thalassemia).
Classification of anemia according to ICD-10
D50 - D53 Anemia associated with nutrition.
D55 - D59 Hemolytic anemia.
D60 - D64 Aplastic and other anemias.
When collecting anamnesis from patients with anemia, it is necessary to ask:
About recent bleeding;
New pallor;
Severity of menstrual bleeding;
Diet and alcohol consumption;
Loss of body weight (>7 kg for 6 months);
Presence of anemia in the family history;
A history of gastrectomy (if vitamin B12 deficiency is suspected) or intestinal resection;
Pathological symptoms from the upper gastrointestinal tract (dysphagia, heartburn, nausea, vomiting);
Pathological symptoms from the lower gastrointestinal tract (changes in the usual functioning of the intestines, bleeding from the rectum, pain that decreases with defecation).
When examining a patient, they look for:
Pallor of the conjunctiva;
Paleness of facial skin;
Pallor of the skin of the palms;
Signs of acute bleeding:
Tachycardia in the supine position (pulse rate >100 per minute);
Hypotension in the supine position (systolic blood pressure<95 мм рт.ст);
Increased heart rate >30 per minute or severe dizziness when moving from a lying position to a sitting or standing position;
Signs of heart failure;
Jaundice (hemolytic or sideroblastic anemia can be assumed);
Signs of infection or spontaneous bruising (suggestive of bone marrow failure);
Tumor-like formations in the abdominal cavity or rectum:
An examination of the patient's rectum and a test for occult blood in feces are performed.
Research to be done
Blood cell count and blood smear.
Determination of blood type and creation of a patient’s own blood bank.
Determination of urea concentration and electrolyte content.
Functional liver tests.
Determining SES and SSGE can help in identifying potential causes of anemia (Table 192).
Table 192. Causes of anemia
Average red blood cell volume
SEA (MCV - mean corpuscular volume)- average corpuscular volume - the average volume of red blood cells, measured in femtoliters (fl) or cubic micrometers. In hematology analyzers, SER is calculated by dividing the sum of cell volumes by the number of red blood cells, but this parameter can be calculated using the formula:
Ht (%) 10
RBC (10 12 /l)
Average erythrocyte volume values characterizing an erythrocyte:
80-100 fl - normocyte;
-<80 fl - микроцит;
->100 fl - macrocyte.
SES (Table 193) cannot be reliably determined if the test blood contains a large number of abnormal red blood cells (for example, sickle cells) or a dimorphic population of red blood cells.
Table 193. Average erythrocyte volume (Tietz N., 1997)
The average volume of an erythrocyte is 80-97.6 microns.
The clinical significance of SES is similar to the value of unidirectional changes in the color index and hemoglobin content in the erythrocyte (MCI), since macrocytic anemias are usually
at the same time hyperchromic (or normochromic), and microcytic - hypochromic. SES is used mainly to characterize the type of anemia (Table 194).
Table 194. Diseases and conditions accompanied by changes in the average erythrocyte volume
Changes in SER provide information about disturbances in the water-electrolyte balance: an increased value of SER indicates a hypotonic nature of the disturbances in water-electrolyte balance, a decrease indicates a hypertonic nature.
Average hemoglobin content in an erythrocyte (Table 195)
Table 195. Average hemoglobin content in an erythrocyte (Tietz N., 1997)
End of table. 195
The average hemoglobin content in an erythrocyte is 26-33.7 pg.
MCH has no independent meaning and is always correlated with SES, color indicator and average hemoglobin concentration in erythrocytes (MCHC). Based on these indicators, normo-, hypo- and hyperchromic anemias are distinguished.
A decrease in MCH (i.e. hypochromia) is characteristic of hypochromic and microcytic anemia, including iron deficiency, anemia in chronic diseases, thalassemia; with some hemoglobinopathies, lead poisoning, impaired porphyrin synthesis.
An increase in MCH (i.e. hyperchromia) is observed in megaloblastic, many chronic hemolytic anemias, hypoplastic anemia after acute blood loss, hypothyroidism, liver diseases, metastases of malignant neoplasms; when taking cytostatics, contraceptives, anticonvulsants.
Four main functions of iron
enzymes
Electron transport (cytochromes, iron sulfur proteins).
Transport and storage of oxygen (hemoglobin, myoglobin).
Participation in the formation of active centers of redox enzymes (oxidase, hydroxylase, superoxide dismutase, etc.).
Transport and deposition of iron (transferrin, hemosiderin, ferritin).
The level of iron in the blood determines the condition of the body (Table 196,
197).
Table 196. Serum iron content is normal (Tits N., 2005)
Table 197. The most important diseases, syndromes, signs of iron deficiency and excess in the human body (Avtsyn A.P., 1990)
Necessary research
Microcytic anemia: - ± serum ferritin.
Macrocytic anemia:
Serum folic acid;
Vitamin B 12 (cobalamin) in blood serum;
-± methylmalonic acid in urine or serum (if vitamin B 12 deficiency is suspected).
Subsequent studies
Iron-deficiency anemia:
Gastroscopy and colonoscopy.
Vitamin B 12 deficiency
Antibodies to Castle factor.
Schilling test.
Iron-deficiency anemia
In 2/3 of cases, anemia occurs due to diseases of the upper sections
Gastrointestinal tract.
Common causes of iron deficiency anemia in the elderly:
Peptic ulcer or erosion;
Neoplasm in the rectal or colon area;
Stomach surgery;
Presence of a hernial opening (>10 cm);
Malignant disease of the upper gastrointestinal tract;
Angiodysplasia;
Varicose veins of the esophagus.
Vitamin B 12 deficiency
Common reasons:
Pernicious anemia;
Tropical sprue;
Bowel resection;
Jejunal diverticulum;
Violation of absorption of vitamin B 12;
Vegetarianism.
Folate deficiency
Common reasons:
Alcoholism;
Malnutrition.
Approved by order of the Ministry of Health and Social Development of the Russian Federation From ____________ No.
Standard of care for patients with gastrointestinal bleeding, unspecified
1. Patient model.
. Nosological form: unspecified gastrointestinal bleeding.
. ICD-10 code: K92.2.
. Phase: acute condition.
. Stage: first appeal.
. Complications: regardless of complications.
. Terms of service: emergency.
Diagnostics
Treatment at the rate of 20 minutes
Chronic posthemorrhagic anemia
End of table.
*ATH - anatomical-therapeutic-chemical classification. **ODD - approximate daily dose. ***ECD - equivalent course dose.
CLINICAL EXAMINATION
Patient V., 58 years old, complained of general weakness, fatigue, periodic dizziness, tinnitus, flashing “spots” before the eyes, drowsiness during the daytime. He notes that lately he has been feeling the urge to eat chalk.
From the anamnesis
Over the past two years, the patient switched to a vegetarian diet.
Objectively: the skin and visible mucous membranes are pale, the nails are thinned. Peripheral lymph nodes are not enlarged. In the lungs there is vesicular breathing, no wheezing. Heart sounds are muffled, rhythmic, systolic murmur at the apex. Heart rate 80 per minute. Blood pressure 130/75 mm Hg. Art. The tongue is moist and covered with a white coating. The abdomen is soft and painless on palpation.
The patient was examined
General blood analysis
Hemoglobin - 85 g/l, erythrocytes - 3.4x10 12 /l, color index - 0.8, hematocrit - 27%, leukocytes - 5.7x10 9 /l, band - 1, segmented - 72, lymphocytes - 19, monocytes - 8, platelets - 210x10 9 /l, anisochromia and poikilocytosis are noted.
MCH (average hemoglobin content in a red blood cell) is 24.9 pg (normal is 27-35 pg).
MSHC - 31.4% (normal 32-36%). SEO - 79.4 microns (norm 80-100 microns).
Blood chemistry
Iron in blood serum - 10 µmol/l (normal 12-25 µmol/l).
The total iron-binding capacity of serum is 95 µmol/l (normal 30-86 µmol/l).
The percentage of transferrin saturation with iron is 10.5% (normal
16-50%).
Fibrogastroduodenoscopy
Conclusion: superficial gastroduodenitis.
Colonoscopy. Conclusion: no pathology was identified.
Consultation with an obstetrician-gynecologist. Conclusion: menopause 5 years. Atrophic colpitis.
Based on the patient’s complaints (general weakness, fatigue, periodic dizziness, tinnitus, floaters before the eyes, drowsiness during the day, desire to eat chalk) and laboratory examination data [in the general blood test, the content of hemoglobin and red blood cells is reduced; the size of the red blood cells is reduced, of different shapes, different in color intensity (signs of irritation of the erythrocyte germ); a biochemical blood test shows a decrease in iron content in the blood serum, an increase in the total iron-binding capacity of serum, a decrease in the percentage of transferrin saturation with iron and a decrease in serum ferritin] the patient was diagnosed with moderate iron deficiency anemia (of nutritional origin).
RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2013
Iron deficiency anemia, unspecified (D50.9)
Hematology
general information
Short description
Approved by the minutes of the meeting
Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan
No. 23 from 12/12/2013
Iron deficiency anemia (IDA)- clinical-hematological syndrome, characterized by impaired hemoglobin synthesis as a result of iron deficiency, developing against the background of various pathological (physiological) processes, and manifested by signs of anemia and sideropenia (L.I. Dvoretsky, 2004).
Protocol name:
IRON-DEFICIENCY ANEMIA
Protocol code:
ICD-10 code(s):
D 50 Iron deficiency anemia
D 50.0 Posthemorrhagic (chronic) anemia
D 50.8 Other iron deficiency anemias
D 50.9 Iron deficiency anemia, unspecified
Date of protocol development: 2013
Abbreviations used in the protocol:
ID - iron deficiency
DNA - deoxyribonucleic acid
IDA - iron deficiency anemia
IDS - iron deficiency state
CPU - color index
Protocol users: hematologist, therapist, gastroenterologist, surgeon, gynecologist
Classification
There is currently no generally accepted classification of iron deficiency anemia.
Clinical classification of iron deficiency anemia (for Kazakhstan).
In the diagnosis of iron deficiency anemia, it is necessary to highlight 3 points:
Etiological form (will be clarified after further examination)
- Due to chronic blood loss (chronic posthemorrhagic anemia)
- Due to increased iron consumption (increased iron requirement)
- Due to insufficient baseline iron levels (in newborns and young children)
- Alimentary (nutritive)
- Due to insufficient absorption in the intestine
- Due to impaired iron transport
Stages
A. Latent: decreased Fe in the blood serum, iron deficiency without clinical anemia (latent anemia)
B. Clinically developed picture of hypochromic anemia.
Severity
Light (Hb content 90-120 g/l)
Average (Hb content 70-89 g/l)
Severe (Hb content below 70 g/l)
Example: Iron deficiency anemia, post-gastroresection, stage B, severe.
Diagnostics
List of main diagnostic measures:
- General blood test (12 parameters)
- Biochemical blood test (total protein, bilirubin, urea, creatinine, ALT, AST, bilirubin and fractions)
- Serum iron, ferritin, TBC, blood reticulocytes
- General urine analysis
List of additional diagnostic measures:
- Fluorography
- Esophagogastroduodenoscopy,
- Ultrasound of the abdominal cavity, kidneys,
- X-ray examination of the gastrointestinal tract according to indications,
- X-ray examination of the chest organs according to indications,
- Fibercolonoscopy,
- Sigmoidoscopy,
- Ultrasound of the thyroid gland.
- Sternal puncture for differential diagnosis, after consultation with a hematologist, according to indications
Diagnostic criteria*** (description of reliable signs of the disease depending on the severity of the process).
1) Complaints and anamnesis:
Information from the anamnesis:
Chronic posthemorrhagic IDA
1. Uterine bleeding . Menorrhagia of various origins, hyperpolymenorrhea (menses more than 5 days, especially when the first menstruation appears before 15 years, with a cycle of less than 26 days, the presence of blood clots for more than a day), impaired hemostasis, abortion, childbirth, uterine fibroids, adenomyosis, intrauterine contraceptives, malignant tumors .
2. Bleeding from the gastrointestinal tract. When chronic blood loss is detected, a thorough examination of the digestive tract “from top to bottom” is carried out, excluding diseases of the oral cavity, esophagus, stomach, intestines, and helminthic infestation by hookworm. In adult men and women after menopause, the main cause of iron deficiency is bleeding from the gastrointestinal tract, which can provoke: peptic ulcer, diaphragmatic hernia, tumors, gastritis (alcoholic or due to treatment with salicylates, steroids, indomethacin). Disturbances in the hemostatic system can lead to bleeding from the gastrointestinal tract.
3. Donation (in 40% of women it leads to hidden iron deficiency, and sometimes, mainly in female donors with many years of experience (more than 10 years) - it provokes the development of IDA.
4. Other blood loss : nasal, renal, iatrogenic, artificially caused by mental illness.
5. Hemorrhages in confined spaces : pulmonary hemosiderosis, glomic tumors, especially with ulceration, endometriosis.
IDA associated with increased iron requirements:
Pregnancy, lactation, puberty and intensive growth, inflammatory diseases, intense sports, treatment with vitamin B 12 in patients with B 12 deficiency anemia.
One of the most important pathogenetic mechanisms for the development of anemia in pregnant women is inadequately low production of erythropoietin. In addition to states of overproduction of proinflammatory cytokines caused by pregnancy itself, their overproduction is possible with concomitant chronic diseases (chronic infections, rheumatoid arthritis, etc.).
IDA associated with impaired iron intake
Poor nutrition with a predominance of flour and dairy products. When collecting anamnesis, it is necessary to take into account dietary habits (vegetarianism, fasting, dieting). In some patients, impaired intestinal iron absorption may be masked by common syndromes such as steatorrhea, sprue, celiac disease, or diffuse enteritis. Iron deficiency often occurs after resection of the intestine, stomach, or gastroenterostomy. Atrophic gastritis and concomitant achlorhydria can also reduce iron absorption. Poor absorption of iron can be contributed to by a decrease in the production of hydrochloric acid and a decrease in the time required for the absorption of iron. In recent years, the role of Helicobacter pylori infection in the development of IDA has been studied. It has been noted that in some cases, iron metabolism in the body during Helicobacter eradication can be normalized without additional measures.
IDA associated with impaired iron transport
These IDA are associated with congenital antransferrinemia, the presence of antibodies to transferrin, and a decrease in transferrin due to a general protein deficiency.
a. General anemic syndrome:weakness, increased fatigue, dizziness, headaches (usually in the evening), shortness of breath during exercise, palpitations, syncope, flashing “flies” before the eyes with low blood pressure, a moderate increase in temperature is often observed, often drowsiness during the day and poor falling asleep at night, irritability, nervousness, conflict, tearfulness, decreased memory and attention, decreased appetite. The severity of complaints depends on adaptation to anemia. A slow pace of anemization contributes to better adaptation.
b. Sideropenic syndrome:
- changes in the skin and its appendages(dryness, peeling, easy cracking, pallor). Hair is dull, brittle, “split”, turns gray early, falls out rapidly, changes in nails: thinning, brittleness, transverse striations, sometimes spoon-shaped concavity (koilonychia).
- Changes in mucous membranes(glossitis with atrophy of the papillae, cracks in the corners of the mouth, angular stomatitis).
- Changes in the gastrointestinal tract(atrophic gastritis, atrophy of the esophageal mucosa, dysphagia). Difficulty swallowing dry and solid foods.
- Muscular system. Myasthenia gravis (due to weakening of the sphincters, an imperative urge to urinate, the inability to hold urine when laughing, coughing, and sometimes bedwetting in girls). The consequence of myasthenia gravis can be miscarriage, complications during pregnancy and childbirth (decreased contractility of the myometrium
Predilection for unusual smells.
Perversion of taste. Expressed in the desire to eat something inedible.
- Sideropenic myocardial dystrophy- tendency to tachycardia, hypotension.
- Immune system disorders(the level of lysozyme, B-lysines, complement, some immunoglobulins decreases, the level of T- and B-lymphocytes decreases, which contributes to a high infectious morbidity in IDA and the appearance of secondary immunodeficiency of a combined nature).
2) physical examination:
. pallor of the skin and mucous membranes;
. “blueness” of the sclera due to their degenerative changes, slight yellowness of the area of the nasolabial triangle, palms as a result of impaired carotene metabolism;
. koilonychia;
. cheilitis (seizures);
. vague symptoms of gastritis;
. involuntary urination (due to sphincter weakness);
. symptoms of damage to the cardiovascular system: palpitations, shortness of breath, chest pain and sometimes swelling in the legs.
3) laboratory tests
Laboratory indicators for IDA
| Laboratory indicator | Norm | Changes in IDA | |
| 1 | Morphological changes in red blood cells |
normocytes - 68% microcytes - 15.2% macrocytes - 16.8% |
Microcytosis is combined with anisocytosis, poikilocytosis, anulocytes, plantocytes are present |
| 2 | Color index | 0,86 -1,05 | Hypochromia indicator less than 0.86 |
| 3 | Hemoglobin content |
Women - at least 120 g/l Men - at least 130 g/l |
Reduced |
| 4 | MSN | 27-31 pg | Less than 27 pg |
| 5 | ICSU | 33-37% | Less than 33% |
| 6 | MCV | 80-100 fl | Reduced |
| 7 | RDW | 11,5 - 14,5% | Increased |
| 8 | Average red blood cell diameter | 7.55±0.099 µm | Reduced |
| 9 | Reticulocyte count | 2-10:1000 | Not changed |
| 10 | Effective erythropoiesis coefficient | 0.06-0.08x10 12 l/day | Not changed or reduced |
| 11 | Serum iron |
Women - 12-25 µml/l Men -13-30 µmol/l |
Reduced |
| 12 | Total iron binding capacity of blood serum | 30-85 µmol/l | Promoted |
| 13 | Latent iron binding capacity of serum | Less than 47 µmol/l | Above 47 µmol/l |
| 14 | Transferrin saturation with iron | 16-15% | Reduced |
| 15 | Desferal test | 0.8-1.2 mg | Decrease |
| 16 | Content of protoporphyrins in erythrocytes | 18-89 µmol/l | Increased |
| 17 | Iron painting | Sideroblasts are present in the bone marrow | Disappearance of sideroblasts in punctate |
| 18 | Ferritin level | 15-150 µg/l | Decrease |
4) instrumental studies (x-ray signs, endoscopy - picture).
In order to identify sources of blood loss and pathology of other organs and systems:
- X-ray examination of the gastrointestinal tract according to indications,
- X-ray examination of the chest organs according to indications,
- fibrocolonoscopy,
- sigmoidoscopy,
- Ultrasound of the thyroid gland.
- Sternal puncture for differential diagnosis
5) indications for consultation with specialists:
gastroenterologist - bleeding from the gastrointestinal tract;
dentist - bleeding from gums,
ENT - nosebleeds,
oncologist - a malignant lesion that causes bleeding,
nephrologist - exclusion of kidney diseases,
phthisiatrician - bleeding due to tuberculosis,
pulmonologist - blood loss due to diseases of the bronchopulmonary system, gynecologist - bleeding from the genital tract,
endocrinologist - decreased thyroid function, presence of diabetic nephropathy,
hematologist - to exclude diseases of the blood system, ineffectiveness of ferrotherapy
proctologist - rectal bleeding,
infectious disease specialist - if there are signs of helminthiasis.
Differential diagnosis
| Criteria | ZhDA | MDS (RA) | B12-deficient | Hemolytic anemia | |
| Hereditary | AIGA | ||||
| Age | Most often young, under 60 years old |
Over 60 years old |
Over 60 years old | - | After 30 years |
| Shape of red blood cells | Anisocytosis, poikilocytosis | Megalocytes | Megalocytes | Sphero-, ovalocytosis | Norm |
| Color index | Reduced | Normal or elevated | Promoted | Norm | Norm |
| Price-Jones curve | Norm | Shift right or normal | Shift right | Norm or shift right | Shift left |
| Lifespan of Erythr. | Norm | Normal or shortened | Shortened | Shortened | Shortened |
| Coombs test | Negative | Negative sometimes positive | Negative | Negative | Positive |
| Osmotic resistance Er. | Norm | Norm | Norm | Promoted | Norm |
| Peripheral blood reticulocytes |
Relates. increase, absolute decrease |
Decreased or increased |
Demoted on days 5-7 of treatment, reticulocyte crisis |
Increased | Increase |
| Peripheral blood leukocytes | Norm | Reduced | Possible downgrade | Norm | Norm |
| Peripheral blood platelets | Norm | Reduced | Possible downgrade | Norm | Norm |
| Serum iron | Reduced | Increased or normal | Increased | Increased or normal | Increased or normal |
| Bone marrow | Increase in polychromatophiles | Hyperplasia of all hematopoietic germs, signs of cell dysplasia | Megaloblasts | Increased erythropoiesis with increasing mature forms | |
| Blood bilirubin | Norm | Norm | Possible promotion | Increase in indirect bilirubin fraction | |
| Urobilin urine | Norm | Norm | Possible appearance | Persistent increase in urine urobilin | |
Differential diagnosis of iron deficiency anemia is carried out with other hypochromic anemias caused by impaired hemoglobin synthesis. These include anemia associated with impaired porphyrin synthesis (anemia due to lead poisoning, congenital disorders of porphyrin synthesis), as well as thalassemia. Hypochromic anemia, unlike iron deficiency anemia, occurs with a high content of iron in the blood and depot, which is not used for the formation of heme (sideroachresia); in these diseases there are no signs of tissue iron deficiency.
The differential sign of anemia caused by impaired porphyrin synthesis is hypochromic anemia with basophilic punctation of erythrocytes, reticulocytes, enhanced erythropoiesis in the bone marrow with a large number of sideroblasts. Thalassemia is characterized by a target-like shape and basophilic punctation of erythrocytes, reticulocytosis and the presence of signs of increased hemolysis
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Treatment
Treatment goals:
- Correction of iron deficiency.
- Comprehensive treatment of anemia and complications associated with it.
- Elimination of hypoxic conditions.
- Normalization of hemodynamics, systemic, metabolic and organ disorders.
Treatment tactics***:
non-drug treatment
In case of iron deficiency anemia, the patient is advised to eat a diet rich in iron. The maximum amount of iron that can be absorbed from food in the gastrointestinal tract is 2 g per day. Iron from animal products is absorbed in the intestines in much larger quantities than from plant products. Bivalent iron, which is part of heme, is best absorbed. Meat iron is absorbed better, but liver iron is absorbed worse, since iron in the liver is contained mainly in the form of ferritin, hemosiderin, and also in the form of heme. Iron is absorbed in small quantities from eggs and fruits. The patient is recommended the following foods containing iron: beef, fish, liver, kidneys, lungs, eggs, oatmeal, buckwheat, beans, porcini mushrooms, cocoa, chocolate, greens, vegetables, peas, beans, apples, wheat, peaches, raisins , prunes, herring, hematogen. It is advisable to take kumis in a daily dose of 0.75-1 l, with good tolerance - up to 1.5 l. In the first two days, the patient is given no more than 100 ml of kumis at each dose; from the 3rd day, the patient takes 250 ml 3-4 times a day. It is better to take kumys 1 hour before and 1 hour after breakfast, 2 hours before and 1 hour after lunch and dinner.
In the absence of contraindications (diabetes mellitus, obesity, allergies, diarrhea), the patient should be recommended honey. Honey contains up to 40% fructose, which helps increase the absorption of iron in the intestines. Iron is best absorbed from veal (22%), from fish (11%); 3% of iron is absorbed from eggs, beans, and fruits, and 1% from rice, spinach, and corn.
drug treatment
List separately
- list of essential medicines
- list of additional medicines
***in these sections it is necessary to provide a link to a source that has a good evidence base, indicating the level of reliability. Links should be indicated in the form of square brackets, numbered as they appear. This source must be indicated in the list of references under the appropriate number.
Treatment of IDA should include the following steps:
- Relief of anemia.
B. Saturation therapy (restoration of iron reserves in the body).
B. Maintenance therapy.
The inclusion of ascorbic acid in iron salt preparations improves its absorption. For iron (III) hydroxide polymaltose, the dose may be higher, approximately 1.5 times relative to the latter, because The drug is non-ionic and is tolerated significantly better than iron salts, while only the amount of iron that the body needs is absorbed and only through the active route.
It should be noted that iron is better absorbed when the stomach is “empty”, so it is recommended to take the drug 30-60 minutes before meals. With adequate administration of iron supplements in a sufficient dose, a rise in reticulocytes is noted on days 8-12, and the Hb content increases by the end of the 3rd week. Normalization of red blood counts occurs only after 5-8 weeks of treatment.
All iron preparations are divided into two groups:
1. Ionic iron-containing preparations (salt, polysaccharide compounds of ferrous iron - Sorbifer, Ferretab, Tardiferon, Maxifer, Ranferon-12, Aktiferin, etc.).
2. Nonionic compounds, which include ferric iron preparations, represented by the iron-protein complex and the hydroxide-polymaltose complex (Maltofer). Iron (III)-hydroxide polymaltose complex (Venofer, Cosmofer, Ferkail)
Table. Basic iron preparations for oral administration
| A drug | Additional components | Dosage form | Amount of iron, mg |
| Monocomponent drugs | |||
| Aristopheron | ferrous sulfate |
syrup - 200 ml, 5 ml - 200 mg |
|
| Ferronal | ferrous gluconate | tab., 300 mg | 12% |
| Ferrogluconate | ferrous gluconate | tab., 300 mg | 12% |
| Hemophere prolongatum | ferrous sulfate | tab., 325 mg | 105 mg |
| Iron wine | iron sucrose |
solution, 200 ml 10 ml - 40 mg |
|
| Heferol | ferrous fumarate | capsules, 350 mg | 100 mg |
| Combination drugs | |||
| Aktiferin |
Ferrous sulfate, D,L-serine ferrous sulfate, D,L-serine, glucose, fructose ferrous sulfate, D,L-serine, glucose, fructose, potassium sorbate |
caps., 0.11385 g syrup, 5 ml-0.171 g drops, 1 ml - 0.0472 g |
0.0345 g 0.034 g 0.0098 g |
| Sorbifer - durules |
ferrous sulfate, ascorbic acid acid |
tab., 320 mg | 100 mg |
| Ferrstab | tab., 154 mg | 33% | |
| Folfetab | Ferrous fumarate, folic acid | tab., 200 mg | 33% |
| Ferroplect |
ferrous sulfate, ascorbic acid acid |
tab., 50 mg | 10 mg |
| Ferroplex |
ferrous sulfate, ascorbic acid acid |
tab., 50 mg | 20% |
| Fefol | ferrous sulfate, folic acid | tab., 150 mg | 47 mg |
| Ferro-foil |
ferrous sulfate, folic acid, cyanocobalamin |
caps., 100 mg | 20% |
| Tardiferon - retard | ferrous sulfate, ascorbic acid | dragee, 256.3 mg | 80 mg |
| acid, mucoproteosis | |||
| Gyno-tardiferon |
ferrous sulfate, ascorbic acid acid, mucoproteosis, folic acid |
dragee, 256.3 mg | 80 mg |
| 2Macrofer | Ferrous gluconate, folic acid |
effervescent tablets, 625 mg |
12% |
| Fenyuls |
ferrous sulfate, ascorbic acid acid, nicotinamide, vitamins Group B |
caps., | 45 mg |
| Irovit |
ferrous sulfate, ascorbic acid acid, folic acid, cyanocobalamin, lysine monohydro- chloride |
caps., 300 mg | 100 mg |
| Ranferon-12 | Ferrous fumarate, ascorbic acid, folic acid, cyanocobalamin, zinc sulfate | Caps., 300 mg | 100 mg |
| Totema | Iron gluconate, manganese gluconate, copper gluconate | Ampoules with drinking solution | 50 mg |
| Globiron | Ferrous fumarate, folic acid, cyanocobalamin, pyridoxine, sodium docusate | Caps., 300 mg | 100 mg |
| Gemsineral-TD | Ferrous fumarate, folic acid, cyanocobalamin | Caps., 200 mg | 67 mg |
| Ferramin-Vita | Ferrous aspartate, ascorbic acid, folic acid, cyanocobalamin, zinc sulfate | Table, 60 mg | |
| Maltofer |
Drops, syrup, 10 mg Fe in 1 ml; Table chewable 100 mg |
||
| Maltofer Fall | polymaltose hydroxyl iron complex, folic acid | Table chewable 100 mg | |
| Ferrum Lek | polymaltose hydroxyl iron complex | Table chewable 100 mg |
To relieve mild IDA:
Sorbifer 1 tablet. x 2 rub. per day 2-3 weeks, Maxifer 1 tablet. x 2 times a day, 2-3 weeks, Maltofer 1 tablet 2 times a day - 2-3 weeks, Ferrum-lek 1 tablet x 3 r. in the village 2-3 weeks;
Moderate severity: Sorbifer 1 tablet. x 2 rub. per day 1-2 months, Maxifer 1 tablet. x 2 times a day, 1-2 months, Maltofer 1 tablet 2 times a day - 1-2 months, Ferrum-lek 1 tablet x 3 r. in the village 1-2 months;
Severe severity: Sorbifer 1 tablet. x 2 rub. per day 2-3 months, Maxifer 1 tablet. x 2 times a day, 2-3 months, Maltofer 1 tablet 2 times a day - 2-3 months, Ferrum-lek 1 tablet x 3 r. in the village 2-3 months.
Of course, the duration of therapy is influenced by the hemoglobin level during ferrotherapy, as well as the positive clinical picture!
Table. Iron preparations for parenteral administration.
| Trade name | INN | Dosage form | Amount of iron, mg |
| Venofer IV | Iron III hydroxide sucrose complex | Ampoules 5.0 | 100 mg |
| Ferkail v/m | Iron III dextran | Ampoules 2.0 | 100 mg |
| Cosmopher v/m, v/v | Ampoules 2.0 | 100 mg | |
| Novofer-D intramuscularly, intravenously | Iron III hydroxide-dextran complex | Ampoules 2.0 | 100 mg/2ml |
Indications for parenteral administration of iron supplements:
. Intolerance to iron supplements for oral administration;
. Impaired absorption of iron;
. Peptic ulcer of the stomach and duodenum during exacerbation;
. Severe anemia and the vital need to quickly replenish iron deficiency, for example, preparation for surgery (refusal of hemocomponent therapy)
For parenteral administration, ferric iron preparations are used.
The course dose of iron preparations for parenteral administration is calculated using the formula:
A = 0.066 M (100 - 6 Nb),
where A is the course dose, mg;
M—patient’s body weight, kg;
Hb—Hb content in blood, g/l.
IDA treatment regimen:
1. If the hemoglobin level is 109-90 g/l, hematocrit is 27-32%, prescribe a combination of drugs:
A diet that includes iron-rich foods - beef tongue, rabbit meat, chicken, porcini mushrooms, buckwheat or oatmeal, legumes, cocoa, chocolate, prunes, apples;
Salts, polysaccharide compounds of ferrous iron, iron (III)-hydroxide polymaltose complex in a total daily dose of 100 mg (oral administration) for 1.5 months with monitoring of a general blood test once a month, if necessary, extending the course of treatment to 3 months;
Ascorbic acid 2 dr. x 3 r. in the village 2 weeks
2. If the hemoglobin level is below 90 g/l, the hematocrit is below 27%, consult a hematologist.
Salt or polysaccharide compounds of ferrous iron or iron (III)-hydroxide polymaltose complex in a standard dosage. In addition to the previous therapy, prescribe iron (III)-hydroxide polymaltose complex (200 mg/10 ml) intravenously every other day, the amount of administered iron should be calculated according to the formula given in the manufacturer’s instructions or iron III dextran (100 mg/2 ml) once every day, intramuscularly (calculation according to the formula), with individual selection of the course depending on hematological parameters, at this moment the intake of oral iron supplements is temporarily stopped;
3. When the hemoglobin level is normalized to more than 110 g/l and hematocrit to more than 33%, prescribe a combination of preparations of salt or polysaccharide compounds of divalent iron or iron (III)-hydroxide polymaltose complex 100 mg once a week for 1 month, under the control of hemoglobin levels, ascorbic acid 2 dr. x 3 r. per day 2 weeks (not applicable for pathologies of the gastrointestinal tract - erosion and ulcers of the esophagus, stomach), folic acid 1 tablet. x 2 rub. in the village for 2 weeks.
4. If the hemoglobin level is less than 70 g/l, inpatient treatment in the hematology department, if acute gynecological or surgical pathology is excluded. Mandatory preliminary examination by a gynecologist and surgeon.
In case of severe anemic and circulatory-hypoxic syndromes, leukofiltered erythrocyte suspension, further transfusions strictly according to absolute indications, according to the Order of the Minister of Health of the Republic of Kazakhstan dated July 26, 2012 No. 501. On amendments to the order of the acting. Minister of Health of the Republic of Kazakhstan dated November 6, 2009 No. 666 “On approval of the Nomenclature, Rules for the procurement, processing, storage, sale of blood and its components, as well as Rules for the storage, transfusion of blood, its components and preparations”
In the preoperative period, in order to quickly normalize hematological parameters, transfusion of leukofiltered erythrocyte suspension, according to Order No. 501;
Salt or polysaccharide compounds of divalent iron or iron (III)-hydroxide polymaltose complex (200 mg/10 ml) intravenously every other day according to calculations according to the instructions and under the control of hematological parameters.
For example, a scheme for calculating the amount of administered drug relative to Cosmofer:
Total dose (Fe mg) = body weight (kg) x (required Hb - actual Hb) (g/l) x 0.24 + 1000 mg (Fe reserve). Factor 0.24 = 0.0034 (iron content in Hb is 0.34%) x 0.07 (blood volume 7% of body weight) x 1000 (transition from g to mg). Course dose in ml (for iron deficiency anemia) in terms of body weight (kg) and depending on Hb indicators (g/l), which corresponds to:
60, 75, 90, 105 g/l:
60 kg - 36, 32, 27, 23 ml, respectively;
65 kg - 38, 33, 29, 24 ml, respectively;
70 kg - 40, 35, 30, 25 ml, respectively;
75 kg - 42, 37, 32, 26 ml, respectively;
80 kg - 45, 39, 33, 27 ml, respectively;
85 kg - 47, 41, 34, 28 ml, respectively;
90 kg - 49, 42, 36, 29 ml, respectively.
If necessary, treatment is described in stages: emergency care, outpatient, inpatient.
Other treatments- No
Surgical intervention
Indications for surgical treatment are ongoing bleeding, increasing anemia, due to reasons that cannot be eliminated by drug therapy.
Prevention
Primary prevention carried out in groups of people who do not currently have anemia, but there are circumstances predisposing to the development of anemia:
. pregnant and breastfeeding women;
. teenage girls, especially those with heavy menstruation;
. donors;
. women with heavy and prolonged menstruation.
Prevention of iron deficiency anemia in women with heavy and prolonged menstruation.
2 courses of preventive therapy are prescribed for a duration of 6 weeks (the daily dose of iron is 30-40 mg) or after menstruation for 7-10 days every month for a year.
Prevention of iron deficiency anemia in donors and children of sports schools.
1-2 courses of preventive treatment are prescribed for 6 weeks in combination with an antioxidant complex.
During periods of intense growth in boys, iron deficiency anemia may develop. At this time, preventive treatment with iron supplements should also be carried out.
Secondary prevention is performed for persons with previously cured iron deficiency anemia in the presence of conditions that threaten the development of relapse of iron deficiency anemia (heavy menstruation, uterine fibroids, etc.).
For these groups of patients, after treatment of iron deficiency anemia, a preventive course lasting 6 weeks is recommended (daily dose of iron - 40 mg), then two 6-week courses per year or taking 30-40 mg of iron daily for 7-10 days after menstruation are given. In addition, you must consume at least 100 g of meat daily.
All patients with iron deficiency anemia, as well as persons with risk factors for this pathology, must be registered with a general practitioner in the clinic at their place of residence, with a mandatory general blood test and serum iron testing at least 2 times a year. At the same time, clinical observation is also carried out taking into account the etiology of iron deficiency anemia, i.e. The patient is being monitored for a disease that has caused iron deficiency anemia.
Further management
Clinical blood tests should be performed monthly. In case of severe anemia, laboratory monitoring is carried out every week; in the absence of positive dynamics of hematological parameters, an in-depth hematological and general clinical examination is indicated.
Information
Sources and literature
- Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
- List of references: 1. WHO. Official annual report. Geneva, 2002. 2. Iron deficiency anemia assessment, prevention and control. A guide for program managers - Geneva: World Health Organization, 2001 (WHO/NHD/01.3). 3. Dvoretsky L.I. WAITING. Newdiamid-AO. M.: 1998. 4. Kovaleva L. Iron deficiency anemia. M.: Doctor. 2002; 12:4-9. 5. G. Perewusnyk, R. Huch, A. Huch, C. Breymann. British Journal of Nutrition. 2002; 88: 3-10. 6. Strai S.K.S., Bomford A., McArdle H.I. Iron transport across cell membranes: molecular understanding of duodenal and placental iron uptake. Best Practice & Research Clin Haem. 2002; 5:2:243-259. 7. Schaeffer R.M., Gachet K., Huh R., Krafft A. Iron letter: recommendations for the treatment of iron deficiency anemia. Hematology and Transfusiology 2004; 49 (4): 40-48. 8. Dolgov V.V., Lugovskaya S.A., Morozova V.T., Pochtar M.E. Laboratory diagnosis of anemia. M.: 2001; 84. 9. Novik A.A., Bogdanov A.N. Anemia (from A to Z). Guide for doctors / ed. Academician Yu.L. Shevchenko. – St. Petersburg: “Neva”, 2004. – 62-74 p. 10. Papayan A.V., Zhukova L.Yu. Anemia in children: hands. For doctors. – St. Petersburg: Peter, 2001. – 89-127 p. 11. Alekseev N.A. Anemia. – St. Petersburg: Hippocrates. – 2004. – 512 p. 12. Lewis S.M., Bain B., Bates I. Practical and laboratory hematology / trans. from English edited by A.G. Rumyantseva. - M.: GEOTAR-Media, 2009. - 672 p.
Information
List of protocol developers indicating qualification data
A.M. Raisova - head dept. Therapy, Ph.D.
O.R. Khan - assistant at the Department of Postgraduate Therapy, hematologist
Disclosure of no conflict of interest: No
Reviewers:
Specifying the conditions for reviewing the protocol: every 2 years.
Attached files
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In a healthy person, all basic blood values should be normal; any deviation is a sign of the development of 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; pathology always develops against the background of malfunctions in the functioning of 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 of restoration of bone marrow tissue, 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, are attacks of dizziness, drowsiness, increased fatigue, irritability, pale skin, and 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 | Problems with concentration, shortness of breath, irregular heart rhythm, convulsions, and with internal bleeding, the stool becomes black. External signs are jams, white spots on the surface of the nail plates, the skin is peeling, the hair loses its shine, splits, the surface of the tongue is glossy. |
| B12 deficient | Noise in the ears, flashing black spots, rapid heartbeat, 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 of the lower extremities, increased susceptibility to infectious diseases, causeless fever. External manifestations are bleeding gums, ulcers in the mouth, a small red rash, the appearance of bruises even after minor blows, and a jaundiced tint to 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 of 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 is a severe hereditary disease that occurs due to an increase in the rate of hemoglobin formation, red blood cells have the shape of a target. Signs are jaundice, an earthy-green tint of the skin, an irregular shape of the skull and a violation of the structure of bone tissue, abnormalities in mental and physical development, the eyes have a Mongoloid cut, 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 the gall bladder, 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 be carried out. 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;
- examination of stool for the presence of 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 additional therapy after preliminary consultation with the attending physician.
Simple recipes:
- Mix the juice of black radish, carrots, and beets in equal proportions and 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.
- 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.
- To 200 ml of pomegranate juice, add 100 ml of carrot, apple and lemon juice, 70 ml of liquid honey. Place the mixture in the refrigerator for 48 hours. Drink 30 ml three times a day.
- 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.
- 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 treatment against the background of anemia, the immune system is significantly weakened, and 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, and 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, against the background of frequent vomiting due to 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
A proper, balanced diet will help reduce the likelihood of anemia - reduce the consumption of animal fats, replace them with vegetable fats, 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 porridge, 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.
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
ICD 10. Class III (D50-D89)
ICD 10. Class III. Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism (D50-D89)
Excluded: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine diseases, nutritional and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), trauma, poisoning and certain other consequences of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)
This class contains the following blocks:
D50-D53 Anemia associated with nutrition
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and hematopoietic organs
D80-D89 Selected disorders involving the immune mechanism
The following categories are marked with an asterisk:
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere
NUTRITION-RELATED ANEMIA (D50-D53)
D50 Iron deficiency anemia
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified
D51 Vitamin B12 deficiency anemia
Excludes: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund(-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with nutrition. Anemia of vegetarians
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
D52 Folate deficiency anemia
D52.0 Folate deficiency anemia associated with nutrition. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia, drug-induced. If necessary, identify the drug
use an additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folate deficiency anemia, unspecified. Anemia due to insufficient intake of folic acid, NOS
D53 Other diet-related anemias
Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folate
D53.0 Anemia due to protein deficiency. Anemia due to amino acid deficiency.
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: DiGuglielmo disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified anemias associated with nutrition.
Anemia associated with deficiency:
Excludes: malnutrition without mention of
anemia, such as:
Copper deficiency (E61.0)
Molybdenum deficiency (E61.5)
Zinc deficiency (E60)
D53.9 Diet-related anemia, unspecified. Simple chronic anemia.
Excludes: anemia NOS (D64.9)
HEMOLYTIC ANEMIA (D55-D59)
D55 Anemia due to enzyme disorders
Excludes: drug-induced enzyme deficiency anemia (D59.2)
D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6PD deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (except G-6-PD) associated with hexose monophosphate [HMP]
bypass of the metabolic pathway. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Hemolytic non-spherocytic (hereditary) type II
Due to hexokinase deficiency
Due to pyruvate kinase deficiency
Due to triosephosphate isomerase deficiency
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemia due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56 Thalassemia
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta thalassemia. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.
D56.3 Carriage of thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [HFH]
D56.9 Thalassemia, unspecified. Mediterranean anemia (with other hemoglobinopathy)
Thalassemia minor (mixed) (with other hemoglobinopathy)
D57 Sickle cell disorders
Excludes: other hemoglobinopathies (D58. -)
sickle cell beta thalassemia (D56.1)
D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
D57.2 Double heterozygous sickle cell disorders
D57.3 Carriage of the sickle cell trait. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders
D58 Other hereditary hemolytic anemias
D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
D58.8 Other specified hereditary hemolytic anemias. Stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59 Acquired hemolytic anemia
D59.0 Drug-induced autoimmune hemolytic anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (warm type). Chronic disease caused by cold hemagglutinins.
Cold type (secondary) (symptomatic)
Thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified. Chronic idiopathic hemolytic anemia
APLASTIC AND OTHER ANEMIA (D60-D64)
D60 Acquired pure red cell aplasia (erythroblastopenia)
Includes: red cell aplasia (acquired) (adults) (with thymoma)
D60.0 Chronic acquired pure red cell aplasia
D60.1 Transient acquired pure red cell aplasia
D60.8 Other acquired pure red cell 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
Excluded: refractory anemia:
With excess blasts (D46.2)
With transformation (D46.3)
With sideroblasts (D46.1)
No sideroblasts (D46.0)
D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, an additional code is used to identify the disease.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshematopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
DiGuglielmo disease (C94.0)
D64.8 Other specified anemias. Childhood pseudoleukemia. Leukoerythroblastic anemia
BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS
HEMORRHAGIC CONDITIONS (D65-D69)
D65 Disseminated intravascular coagulation [defibration syndrome]
Afibrinogenemia acquired. Consumptive coagulopathy
Diffuse or disseminated intravascular coagulation
Acquired fibrinolytic bleeding
Excluded: defibration syndrome (complicating):
In a newborn (P60)
D66 Hereditary factor VIII deficiency
Factor VIII deficiency (with functional impairment)
Excludes: factor VIII deficiency with vascular disorder (D68.0)
D67 Hereditary factor IX deficiency
Factor IX (with functional impairment)
Thromboplastic plasma component
D68 Other bleeding disorders
Abortion, ectopic or molar pregnancy (O00-O07, O08.1)
Pregnancy, childbirth and the puerperium (O45.0, O46.0, O67.0, O72.3)
D68.0 Von Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular impairment. Vascular hemophilia.
Excludes: hereditary capillary fragility (D69.8)
factor VIII deficiency:
With functional impairment (D66)
D68.1 Hereditary factor XI deficiency. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders caused by anticoagulants circulating in the blood. Hyperheparinemia.
If necessary, identify the anticoagulant used, use an additional external cause code.
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
Vitamin K deficiency
Excludes: vitamin K deficiency in the newborn (P53)
D68.8 Other specified bleeding disorders. Presence of systemic lupus erythematosus inhibitor
D68.9 Coagulation disorder, unspecified
D69 Purpura and other hemorrhagic conditions
Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
lightning purple (D65)
thrombotic thrombocytopenic purpura (M31.1)
D69.0 Allergic purpura.
D69.1 Qualitative platelet defects. Bernard-Soulier syndrome [giant platelets].
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). Thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excludes: thrombocytopenia with absent radius (Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified
OTHER DISEASES OF THE BLOOD AND BLOOD FORMING ORGANS (D70-D77)
D70 Agranulocytosis
Agranulocytic tonsillitis. Children's genetic agranulocytosis. Kostmann's disease
If it is necessary to identify the drug causing the neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)
D71 Functional disorders of polymorphonuclear neutrophils
Defect of the cell membrane receptor complex. Chronic (children's) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis
D72 Other white blood cell disorders
Excludes: basophilia (D75.8)
immune disorders (D80-D89)
preleukemia (syndrome) (D46.9)
D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
Excluded: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.8 Other specified white blood cell disorders.
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). Plasmacytosis
D72.9 White blood cell disorder, unspecified
D73 Diseases of the spleen
D73.0 Hyposplenism. Postoperative asplenia. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.5 Splenic infarction. Splenic rupture is non-traumatic. Torsion of the spleen.
Excludes: traumatic splenic rupture (S36.0)
D73.8 Other diseases of the spleen. Splenic fibrosis NOS. Perisplenitis. Splenitis NOS
D73.9 Disease of the spleen, unspecified
D74 Methemoglobinemia
D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemia. Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified
D75 Other diseases of the blood and hematopoietic organs
Excludes: swollen lymph nodes (R59. -)
hypergammaglobulinemia NOS (D89.2)
Mesenteric (acute) (chronic) (I88.0)
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Decreased plasma volume
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs, unspecified
D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system
Excludes: Letterer-Sieve disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
Histiocytic medullary (C96.1)
D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schueller-Crisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If it is necessary to identify an infectious pathogen or disease, an additional code is used.
D76.3 Other histiocytosis syndromes. Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere.
Splenic fibrosis in schistosomiasis [bilharzia] (B65. -)
SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)
Includes: defects in the complement system, immunodeficiency disorders, excluding disease,
caused by human immunodeficiency virus [HIV] sarcoidosis
Excludes: autoimmune diseases (systemic) NOS (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)
D80 Immunodeficiencies with predominant antibody deficiency
D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Non-familial hypogammaglobulinemia. Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective deficiency of immunoglobulin G subclasses
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with increased levels of immunoglobulin M
D80.6 Antibody deficiency with immunoglobulin levels close to normal or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia of children
D80.8 Other immunodeficiencies with a predominant antibody defect. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified
D81 Combined immunodeficiencies
Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)
D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T- and B-cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell count
D81.3 Adenosine deaminase deficiency
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of the major histocompatibility complex
D81.8 Other combined immunodeficiencies. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency, unspecified. Severe combined immunodeficiency disorder NOS
D82 Immunodeficiencies associated with other significant defects
Excludes: ataxic telangiectasia [Louis-Bart] (G11.3)
D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 Di Georg syndrome. Pharyngeal diverticulum syndrome.
Aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified significant defects
D82.9 Immunodeficiency associated with significant defect, unspecified
D83 Common variable immunodeficiency
D83.0 General variable immunodeficiency with predominant abnormalities in the number and functional activity of B cells
D83.1 General variable immunodeficiency with a predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B- or T-cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified
D84 Other immunodeficiencies
D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. C1 esterase inhibitor deficiency
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified
D86 Sarcoidosis
D86.1 Sarcoidosis of lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.8 Sarcoidosis of other specified and combined localizations. Iridocyclitis in sarcoidosis (H22.1).
Multiple cranial nerve palsies in sarcoidosis (G53.2)
Uveoparotitic fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified
D89 Other disorders involving the immune mechanism, not elsewhere classified
Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
non-engraftment and graft rejection (T86. -)
D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving the immune mechanism, unspecified. Immune disease NOS
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ICD code: D50
Iron-deficiency anemia
Iron-deficiency anemia
ICD code online / ICD code D50 / International Classification of Diseases / Diseases of the blood, hematopoietic organs and selected disorders involving the immune mechanism / Anemia associated with nutrition / Iron deficiency anemia
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