Anemia. Regenerative anemia. Diagnosis of folate deficiency anemia. A. Hemorrhagic anemia
Among diseases of the hematopoietic organs, the most common is anemia, or anemia. This is a pathological condition in which the hemoglobin content in the blood is reduced, often with a simultaneous decrease in the number of red blood cells.
Anemia may be associated with large blood loss (for example, due to injury), decreased red function bone marrow, insufficient intake of substances necessary for hematopoietic processes into the body, in particular cyanocobalamin or iron, as well as an infectious-toxic effect on the bone marrow.
Based on the color index of the blood, hypochromic and hyperchromic anemia are distinguished (hyperchromic anemia is characterized by a high color index of the blood; unlike hypochromic anemia, the amount of hemoglobin in the blood decreases to a lesser extent than the number of red blood cells).
A common link in the development mechanism of a number of anemias is a decrease in the regenerative capacity of the red bone marrow. The final loss of the bone marrow's ability to produce red blood cells leads to a rapid increase in anemia. The patient may die from it or from an associated infection.
Currently, the following are the most common forms of anemia, which have a unique clinical picture:
- Posthemorrhagic anemia resulting from blood loss.
- Iron deficiency anemia, which develops due to a lack of iron in the body.
- Pernicious anemia associated with a deficiency of the antianemic factor (cyanocobalamin).
- Hemolytic anemia resulting from the breakdown of red blood cells.
- Hypoplastic anemia, which develops when bone marrow function is suppressed.
In case of anemia that has arisen due to acute and especially large blood loss, the following clinical picture is observed: quite severe general state patient, severe weakness, tinnitus, shortness of breath, palpitations, heaviness in the heart, chilliness, blurred vision, thirst (tissue dehydration), frequent fainting, and in severe cases - collapse, severe pallor. The patient's skin does not have a icteric tint (this is characteristic of hemolytic anemia), a peculiar light blue tint of the sclera attracts attention, and the pupils are dilated. The pulse is frequent, weak, sometimes arrhythmic, blood pressure is low. Skin turgor is reduced. There is yawning involuntary urination, vomit. Body temperature is reduced. On auscultation of the heart, a systolic murmur (in this case called anemic) is noted.
Anemia is hypochromic in nature. It should be noted that when examining blood in the first hours, the content of hemoglobin and red blood cells is almost unchanged, and then decreases.
Blood coagulation is accelerated, leukocytosis and reticulocytosis are determined. The hematocrit number decreases - the ratio of the volume of blood cells to the volume of plasma. The hematocrit number is determined by centrifuging blood under conditions that prevent its clotting in a special device - hematocrit, and normally the volume of red blood cells per unit volume of blood is equal to approximately the volume of the liquid part (45:55), which is associated with the entry of fluid from tissues into the bloodstream (a kind of compensation).
With anemia resulting from repeated frequent blood loss, the general condition of the patient changes little. On examination, pallor is noted, the main complaint is weakness and dizziness. At the onset of the disease, the bone marrow acquires the ability to quickly replenish blood and it retains its normal composition for a long time. Gradually, bone marrow function decreases and sharply hypochromic anemia occurs (characterized by a low blood color index).
Iron-deficiency anemia
The lack of iron in the human body is associated with a number of reasons: lack of iron in food, impaired absorption of iron in the digestive system, etc. As a result, iron deficiency anemia develops. There are the following forms of iron deficiency anemia: late chlorosis and early chlorosis (pale sickness).
Late chlorosis occurs in women mainly 30-45 years old due to impaired iron absorption due to reduced content in the stomach of hydrochloric acid (hydrochloric acid promotes normal absorption of iron). Usually associated with uterine or other bleeding. In addition to the clinical manifestations common to anemia, patients suffering from late chlorosis experience a perversion of taste (the desire to eat chalk, clay, ash, etc.) and a decrease in appetite. On examination - severe pallor, nutrition is not reduced. There are also stomatitis, tongue atrophy, severe pathological changes stomach and intestines (decreased secretory function of the stomach up to achylia), severe functional disorders small intestine, accompanied by diarrhea.
A blood test shows that with a moderate decrease in the number of red blood cells, the amount of hemoglobin decreases significantly. This type of anemia is classified as hypochromic anemia. The red blood cells in the smear are poorly stained, their diameter is reduced, and the number of white blood cells is within normal limits.
Early chlorosis, or pale sickness, is the result of hormonal disorders, in particular a decrease in the stimulating effect of ovarian hormones on the bone marrow. The onset of the disease dates back to puberty. The clinical picture has some features: the skin is pale with a greenish tint, the skin almost does not tan, and some neuropsychic instability appears. This anemia is also hypochromic.
Iron deficiency anemia also includes chlorosis in pregnant women, anemia after gastric resection, etc.
Pernicious anemia
Previously, this disease was called pernicious anemia (Addison-Birmer disease, named after the researchers who first described this disease), since there was no specific treatment and often death occurred. It is currently known that the main cause of pernicious anemia is the lack and impaired absorption of cyanocobalamin (vitamin B12) in the body, which is associated not only with poor nutrition (cyanocobalamin is found in meat and dairy products, eggs), but also with the absence of special substance- gastromucoprotein. Normally, this substance is contained in the stomach and during the atrophic process in its mucous membrane it disappears (a pathogenetic connection has been established between pernicious anemia and chronic gastritis). As a result, the maturation of red blood cells is disrupted. The role of heredity in the development of the disease cannot be ruled out. Many organs are involved in the pathological process.
Symptoms of pernicious anemia
Symptoms of pernicious anemia. The disease develops gradually, often starting after an infection (flu). Middle-aged people (35-60 years old) are more likely to get sick. Patients complain of gradually increasing weakness, burning of the tongue, numbness and tingling sensation at the ends of the fingers, impaired sensitivity of the skin and other parts of the body, muscle pain, loss of appetite, belching, sometimes vomiting, diarrhea, etc. On examination, pallor is noted. skin, petechiae. The tongue has a peculiar appearance: it is bright red, with smoothed papillae, sometimes with ulcerations. Body temperature is often elevated. On auscultation of the heart, a systolic murmur is noted above the apex, and sometimes there are signs of cardiovascular failure.
Blood changes are indicative. Pernicious anemia is hyperchromic: the color index is higher than one (with a decrease in the total number of erythrocytes, the hemoglobin content in them is increased), large erythrocytes are found - macrocytes, as well as poikilocytes - erythrocytes are not of the usual, round, but of irregular shape (in the form of a cylinder, oval and etc.). The number of leukocytes is reduced (leukopenia).
The disease occurs with a certain cyclicity, exacerbation is more often observed in the spring.
Before the introduction of specific treatment (liver drugs, cyanocobalamin), the disease was incurable and ended in death. Currently, treatment with appropriate courses (see below) leads to recovery. If treatment is delayed or the patient fails to follow medical recommendations, complications may develop. The most severe of them is coma, and occasionally there is paralysis as a result of damage to the spinal cord.
Pernicious anemia can not only be an independent disease, but also develop after surgical removal of the stomach (for various reasons), when infected with a broad tapeworm. Patients complain of indigestion, burning sensation in the tongue, numbness in the fingers and toes, muscle pain, and gait disturbance. The skin is pale, the tongue has smoothed papillae, and achylia is observed when examining gastric juice.
Pressing on the sternum is painful. There may be an increase in body temperature. Blood changes are characteristic. Hyperchromia is pronounced (see above), red blood cells are “oversaturated” with hemoglobin. There are erythrocytes of a changed shape, the number of leukocytes is reduced.
Clinical picture. Sometimes the disease is detected from the first days of life, but more often during puberty. The patient complains of weakness, decreased performance, pain in the right and left hypochondrium, and occasional attacks of chills with increased body temperature.
The skin is pale, slightly jaundiced, the spleen is enlarged and painful on palpation, and with a long course of the disease, an enlargement of the liver is also noted.
During the course of the disease there may be periods of mild clinical manifestations and moments sharp deterioration conditions, so-called hemolytic crises ( strong pain in the area of the spleen and liver, an increase in body temperature, accompanied by severe chills, which is associated with the breakdown of blood cells), during this period jaundice intensifies and severe weakness develops.
Hemolytic jaundice is characterized by certain changes in laboratory parameters. A blood test reveals a pronounced decrease (almost 50%) in hemoglobin and a slight decrease in the number of red blood cells (hypochromic anemia), the blood serum is golden in color, the content of bilirubin (indirect) is increased to 290.8-307.9 µmol/l (normal - 17 .1 µmol/l).
The so-called osmotic stability of red blood cells decreases (normally, hemolysis occurs in a 0.5% solution of sodium chloride, and when the osmotic stability decreases, red blood cells are destroyed in a 0.7% solution). Other changes include the appearance of red blood cells with a smaller diameter than normal, a large number of reticulocytes - more than 10°/oo (the norm is about 10%o). Urine and feces are colored much more intensely than normal (the secretion of urobilin is increased). Moderate jaundice of the skin, pronounced (yellow-brown) coloring of stool, and enlarged spleen are noted.
Hemolytic anemia
There are several points of view regarding the causes of this type of anemia. According to one theory, it is based on an abnormality of hematopoiesis, when red blood cells are characterized by pathological permeability of the membranes and are excessively fragile. According to another theory, hemolytic anemia develops due to the increased function of those organs where hemolysis of red blood cells occurs, which causes their increased breakdown.
Hypoplastic anemia
When the body is exposed to a number of infections and toxic factors, including radioactive substances, the red bone marrow undergoes degeneration (fatty or mucous) and its ability to recover is lost. At less severe lesions hematopoiesis is restored.
Symptoms of hypoplastic anemia. The patient complains of increasing weakness, shortness of breath, loss of appetite, bleeding from the gums and nosebleeds, difficulty swallowing, and a burning sensation in the mouth.
Upon examination, sharp pallor is determined, small pinpoint hemorrhages (petechiae) are visible on the skin and mucous membranes. Body temperature is increased. Phenomena of necrotic tonsillitis are noted - dirty gray deposits are visible in the pharynx, the submandibular and cervical lymph nodes are enlarged. As a result of hematopoietic disorders, granular forms of leukocytes (they have protective function) are either absent or their number decreases, and pathogenic microorganisms easily penetrate the body. This can lead to sepsis with all the clinical manifestations of this disease.
In case of hypoplastic anemia, laboratory tests are of great importance. Blood hemoglobin decreases, severe anemia develops, thrombocytopenia is noted, and bleeding time is significantly prolonged. The number of neutrophil granulocytes is sharply reduced. Severe leukocytopenia occurs (decrease in the number of leukocytes). A significant admixture of blood is found in urine, feces and vomit.
With this disease, the symptoms rapidly increase: a sharp anemia occurs, subcutaneous hemorrhages, hematuria, nasal and gastrointestinal bleeding, bleeding from the gums appear, necrotic processes are observed in the pharynx, and body temperature rises.
A blood test reveals the absence of young forms of red blood cells, a sharp decrease in the content of hemoglobin, neutrophilic granulocytes, acidophilic granulocytes (eosinophils), and a decrease in phagocytic function, which contributes to the progression of sepsis.
In severe cases, death occurs.
Treatment of hypoplastic anemia. In case of posthemorrhagic anemia that has developed as a result of bleeding, the underlying disease is first treated and the cause of anemia is eliminated. A means of strengthening the body is good nutrition- sufficient content of proteins, fats, carbohydrates, vitamins in the diet. Patients benefit from vegetables (primarily carrots), fruits (primarily apples), eggs, dairy products, butter, meat, beef liver, etc. It is necessary to improve hygienic working conditions, especially those associated with occupational hazards.
For medications, iron supplements are used, washed down with diluted hydrochloric acid (for gastric secretory insufficiency). In case of acute blood loss with a rapid decrease in hemoglobin content, transfusion therapy is necessary.
For iron deficiency anemia, juices and iron supplements are prescribed. With late chlorosis, as well as with anemia that develops after gastrectomy, the correct diet and the administration of diluted hydrochloric acid or gastric juice are of great importance. For prevention and treatment (especially chlorosis), a rational work and lifestyle regimen is very important; if necessary, sedatives are prescribed (bromides, valerian preparations).
Treatment of pernicious anemia associated with a lack of cyanocobalamin during exacerbations comes down to the appointment bed rest, nutritious nutrition. The patient should receive raw beef liver (high content of cyanocobalamin) 200-300 g per day.
Cyanocobalamin and thiamine bromide are administered intramuscularly. In some cases, a repeat blood transfusion (250 ml) is given. With proper treatment, complete recovery occurs.
Treatment of hemolytic anemia, if increased hemolysis of red blood cells is caused by intoxication (lead) or infection (malaria), is symptomatic. When this form develops due to an abnormality in hematopoiesis, the spleen is removed. The indication for this operation is severe anemia.
Treatment of hypoplastic anemia gives good results with timely active treatment. It is carried out in a hospital with good care for the sick. Care consists of maintaining oral hygiene, treating with a weak disinfectant solution, and cleaning the skin (prevention of concomitant infections).
Adequate nutrition and blood transfusion (250-400 ml) or red blood cell transfusion (up to 250 ml) are required. For agranulocytosis, sodium nucleinate 1 - 2 ml of a 2-5% solution subcutaneously, antibiotics, hormones, vitamin preparations, liver extract are indicated. Recently, a positive effect has been obtained from the use of pentoxyl, transfusion of leukocytes, and bone marrow transplantation along with other drugs that enhance leukocytosis.
Anemia is a pathological condition of the body, which is characterized by a decrease in the number of red blood cells and hemoglobin per unit of blood. Red blood cells are formed in the red bone marrow from protein fractions and non-protein components under the influence of erythropoietin (synthesized by the kidneys). For three days, red blood cells provide transport mainly of oxygen and carbon dioxide, and nutrients and metabolic products from cells and tissues. The lifespan of a red blood cell is one hundred and twenty days, after which it is destroyed. Old red blood cells accumulate in the spleen, where non-protein fractions are utilized, and protein fractions enter the red bone marrow, participating in the synthesis of new red blood cells.
The entire cavity of the red blood cell is filled with protein, hemoglobin, which includes iron. Hemoglobin gives the red blood cell its red color and also helps it transport oxygen and carbon dioxide. Its work begins in the lungs, where red blood cells enter the bloodstream. Hemoglobin molecules capture oxygen, after which oxygen-enriched red blood cells are sent first through large vessels, and then through small capillaries to each organ, giving cells and tissues the oxygen necessary for life and normal activity.
Anemia weakens the body's ability to exchange gases; due to a reduction in the number of red blood cells, the transport of oxygen and carbon dioxide is disrupted. As a result, a person may experience such signs of anemia as a feeling constant fatigue, loss of strength, drowsiness, and increased irritability.
Anemia is a manifestation of the underlying disease and is not an independent diagnosis. Many diseases, including infectious diseases, benign or malignant tumors may be associated with anemia. This is why anemia is important sign, which requires the necessary research to identify the main cause that led to its development.
Severe forms of anemia due to tissue hypoxia can lead to serious complications, such as states of shock(For example, hemorrhagic shock), hypotension, coronary or pulmonary insufficiency.
Classification of anemia
Anemias are classified:
- by development mechanism;
- by severity;
- by color indicator;
- according to morphological characteristics;
- on the ability of bone marrow to regenerate.
Classification | Description | Kinds |
According to the development mechanism | According to pathogenesis, anemia can develop due to blood loss, impaired formation of red blood cells, or due to their pronounced destruction. | According to the development mechanism there are:
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By severity | Depending on the level of decrease in hemoglobin, three degrees of severity of anemia are distinguished. Normal hemoglobin levels in men are 130–160 g/l, and in women 120–140 g/l. | There are the following degrees of severity of anemia:
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By color index | The color index is the degree of saturation of red blood cells with hemoglobin. It is calculated based on the results of a blood test as follows. The number three must be multiplied by the hemoglobin index and divided by the red blood cell index ( the comma is removed). | Classification of anemia by color indicator:
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According to morphological characteristics | In case of anemia, red blood cells of different sizes may be observed during a blood test. Normally, the diameter of red blood cells should be from 7.2 to 8.0 microns ( micrometer). Smaller size of red blood cells ( microcytosis) can be observed in iron deficiency anemia. Normal size may be present in posthemorrhagic anemia. Larger size ( macrocytosis), in turn, may indicate anemia associated with deficiency of vitamin B12 or folic acid. | Classification of anemia according to morphological characteristics:
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According to the ability of bone marrow to regenerate | Since the formation of red blood cells occurs in the red bone marrow, the main sign of bone marrow regeneration is an increase in the level of reticulocytes ( red blood cell precursors) in blood. Their level also indicates how actively the formation of red blood cells occurs ( erythropoiesis). Normally, in human blood the number of reticulocytes should not exceed 1.2% of all red blood cells. | Based on the ability of bone marrow to regenerate, the following forms are distinguished:
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Causes of anemia
There are three main reasons leading to the development of anemia:
- blood loss (acute or chronic bleeding);
- increased destruction of red blood cells (hemolysis);
- decreased production of red blood cells.
Factors influencing the development of anemia | Causes |
Genetic factor |
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Nutritional factor |
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Physical factor | |
Chronic diseases and neoplasms |
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Infectious factor |
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Pesticides and medications |
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Iron-deficiency anemia
Iron deficiency anemia is hypochromic anemia, which is characterized by a decrease in iron levels in the body. Iron deficiency anemia is characterized by a decrease in red blood cells, hemoglobin and color index.
Iron is a vital element involved in many metabolic processes in the body. A person weighing seventy kilograms has a reserve of iron in the body of approximately four grams. This amount is maintained by maintaining a balance between the regular loss of iron from the body and its intake. To maintain balance daily requirement iron is 20 – 25 mg. Most of the iron entering the body is spent on its needs, the rest is deposited in the form of ferritin or hemosiderin and, if necessary, is consumed.
Causes of iron deficiency anemia
Causes | Description |
Impaired intake of iron into the body |
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Impaired absorption of iron | Iron absorption occurs at the level of the gastric mucosa, so stomach diseases such as gastritis, peptic ulcer or gastric resection lead to impaired iron absorption. |
Increased body need for iron |
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Loss of iron from the body |
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Symptoms of iron deficiency anemia
The clinical picture of iron deficiency anemia is based on the development of two syndromes in the patient:- anemic syndrome;
- sideropenic syndrome.
- severe general weakness;
- increased fatigue;
- attention deficit;
- malaise;
- drowsiness;
- black chair (with gastrointestinal bleeding);
- heartbeat;
- perversion of taste (for example, patients eat chalk, raw meat);
- perversion of the sense of smell (for example, patients sniff acetone, gasoline, paints);
- hair is brittle, dull, split ends;
- white spots appear on the nails;
- the skin is pale, the skin is flaky;
- Cheilitis (seeds) may appear in the corners of the mouth.
Diagnosis of iron deficiency anemia
At medical examination the patient has:- cracks in the corners of the mouth;
- "glossy" language;
- in severe cases, an increase in the size of the spleen.
- microcytosis (small red blood cells);
- hypochromia of erythrocytes (weak coloring of erythrocytes);
- poikilocytosis (red blood cells of different shapes).
- decreased ferritin levels;
- serum iron is reduced;
- The iron-binding capacity of the serum is increased.
To identify the cause that led to the development of anemia, the patient may be prescribed the following instrumental studies:
- fibrogastroduodenoscopy (for examination of the esophagus, stomach and duodenum);
- Ultrasound (for examining the kidneys, liver, female genital organs);
- colonoscopy (to examine the large intestine);
- computed tomography (for example, to study the lungs, kidneys);
- X-rays of light.
Treatment of iron deficiency anemia
Nutrition for anemiaIn nutrition, iron is divided into:
- heme, which enters the body with products of animal origin;
- non-heme, which enters the body with products of plant origin.
Food | Product names | |
Food |
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While following the diet, you should also increase your consumption of foods containing vitamin C, as well as meat protein (they increase the absorption of iron in the body) and reduce the consumption of eggs, salt, caffeine and calcium (they reduce the absorption of iron).
Drug treatment
When treating iron deficiency anemia, the patient is prescribed iron supplements in parallel with the diet. Data medicines designed to replenish iron deficiency in the body. They are available in the form of capsules, dragees, injections, syrups and tablets.
The dose and duration of treatment is selected individually depending on the following indicators:
- patient's age;
- severity of the disease;
- the reasons that caused iron deficiency anemia;
- based on test results.
Iron preparations in the form of injections (intramuscular or intravenous) are used in the following cases:
- with severe anemia;
- if anemia progresses despite taking doses of iron in the form of tablets, capsules or syrup;
- if the patient has diseases of the gastrointestinal tract (for example, gastric and duodenal ulcers, ulcerative colitis, Crohn's disease), since the iron supplement taken may aggravate the existing disease;
- before surgical interventions in order to accelerate the saturation of the body with iron;
- if the patient has intolerance to iron preparations when taken orally.
Surgical intervention is performed if the patient has acute or chronic bleeding. For example, in case of gastrointestinal bleeding, fibrogastroduodenoscopy or colonoscopy can be used to identify the area of bleeding and then stop it (for example, a bleeding polyp is removed, a gastric and duodenal ulcer is coagulated). At uterine bleeding, as well as for bleeding in organs located in the abdominal cavity, laparoscopy can be used.
If necessary, the patient may be prescribed a transfusion of red blood cells to replenish the volume of circulating blood.
B12 – deficiency anemia
This anemia is caused by a lack of vitamin B12 (and possibly folic acid). It is characterized by a megaloblastic type (increased number of megaloblasts, erythrocyte precursor cells) of hematopoiesis and is a hyperchromic anemia. Normally, vitamin B12 enters the body with food. At the level of the stomach, B12 binds to a protein produced in it, gastromucoprotein (internal Castle factor). This protein protects the vitamin entering the body from the negative effects of intestinal microflora, and also promotes its absorption.
The complex of gastromucoproteins and vitamin B12 reaches the distal section (lower section) of the small intestine, where this complex disintegrates, vitamin B12 is absorbed into the intestinal mucosa and then enters the blood.
This vitamin comes from the bloodstream:
- into the red bone marrow to participate in the synthesis of red blood cells;
- to the liver, where it is deposited;
- into the central nervous system for the synthesis of the myelin sheath (covers the axons of neurons).
Causes of B12 deficiency anemia
Exist following reasons development of B12 deficiency anemia:- insufficient intake of vitamin B12 from food;
- disruption of the synthesis of intrinsic factor Castle due to, for example, atrophic gastritis, gastric resection, stomach cancer;
- intestinal damage, for example, dysbiosis, helminthiasis, intestinal infections;
- increased body needs for vitamin B12 ( fast growth, active sports, multiple pregnancy);
- impaired vitamin deposition due to liver cirrhosis.
Symptoms of B12 deficiency anemia
The clinical picture of B12 and folate deficiency anemia is based on the development of the following syndromes in the patient:- anemic syndrome;
- gastrointestinal syndrome;
- neuralgic syndrome.
Syndrome name | Symptoms |
Anemic syndrome |
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Gastrointestinal syndrome |
These symptoms develop due to atrophic changes in the mucous layer of the oral cavity, stomach and intestines. |
Neuralgic syndrome |
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Diagnosis of B12 deficiency anemia
IN general analysis blood the following changes are observed:- decreased levels of red blood cells and hemoglobin;
- hyperchromia (pronounced coloring of red blood cells);
- macrocytosis (increased red blood cell size);
- poikilocytosis (various forms of red blood cells);
- microscopy of erythrocytes reveals Cabot rings and Jolly bodies;
- reticulocytes are reduced or normal;
- decreased level of white blood cells (leukopenia);
- increased levels of lymphocytes (lymphocytosis);
- decreased platelet levels (thrombocytopenia).
Puncture of the red bone marrow reveals an increase in megaloblasts.
The patient may be prescribed the following instrumental studies:
- examination of the stomach (fibrogastroduodenoscopy, biopsy);
- intestinal examination (colonoscopy, irrigoscopy);
- Ultrasound examination of the liver.
Treatment of B12 deficiency anemia
All patients are hospitalized in the hematology department, where they undergo appropriate treatment.Nutrition for B12-deficiency anemia
Diet therapy is prescribed, in which the consumption of foods rich in vitamin B12 is increased.
The daily requirement of vitamin B12 is three micrograms.
Drug treatment
Drug treatment is prescribed to the patient according to the following scheme:
- For two weeks, the patient receives 1000 mcg of Cyanocobalamin intramuscularly daily. Within two weeks, the patient's neurological symptoms disappear.
- Over the next four to eight weeks, the patient receives 500 mcg daily intramuscularly to saturate the vitamin B12 depot in the body.
- Subsequently, the patient receives lifelong intramuscular injections once a week 500 mcg.
A patient with B12-deficiency anemia should be monitored for life by a hematologist, gastrologist and family doctor.
Folate deficiency anemia
Folate deficiency anemia is a hyperchromic anemia characterized by a lack of folic acid in the body. Folic acid (vitamin B9) is a water-soluble vitamin that is partly produced by intestinal cells, but mainly must come from outside to replenish the body's requirements. The daily intake of folic acid is 200 - 400 mcg.
In food products, as well as in body cells folic acid is in the form of folates (polyglutamates).
Folic acid plays an important role in the human body:
- participates in the development of the body in the prenatal period (promotes the formation of nerve conduction of tissues, circulatory system fetus, prevents the development of certain malformations);
- participates in the growth of the child (for example, in the first year of life, during puberty);
- affects hematopoietic processes;
- together with vitamin B12, participates in DNA synthesis;
- prevents the formation of blood clots in the body;
- improves the processes of regeneration of organs and tissues;
- participates in tissue renewal (for example, skin).
Causes of folate deficiency anemia
There are the following reasons for the development of folate deficiency anemia:- insufficient intake of folic acid from food;
- increased loss of folic acid from the body (for example, with cirrhosis of the liver);
- impaired absorption of folic acid in the small intestine (for example, with celiac disease, when taking certain medications, with chronic alcohol intoxication);
- increased body needs for folic acid (for example, during pregnancy, malignant tumors).
Symptoms of folate deficiency anemia
With folate deficiency anemia, the patient experiences anemic syndrome (symptoms such as increased fatigue, palpitations, pale skin, decreased performance). Neurological syndrome, as well as atrophic changes in the mucous membrane of the oral cavity, stomach and intestines are absent with this type of anemia.The patient may also experience an increase in the size of the spleen.
Diagnosis of folate deficiency anemia
During a general blood test, the following changes are observed:- hyperchromia;
- decreased levels of red blood cells and hemoglobin;
- macrocytosis;
- leukopenia;
- thrombocytopenia.
A myelogram reveals an increased content of megaloblasts and hypersegmented neutrophils.
Treatment of folate deficiency anemia
Nutrition plays an important role in folate deficiency anemia; the patient needs to consume foods rich in folic acid every day.It should be noted that during any cooking, folates are destroyed by approximately fifty percent or more. Therefore, to provide the body with the necessary daily intake, it is recommended to consume fresh foods (vegetables and fruits).
| Food | Product Name | Amount of iron per hundred milligrams |
| Food of animal origin |
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| Food products of plant origin |
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Drug treatment for folate deficiency anemia includes taking folic acid in amounts of five to fifteen milligrams per day. Required dosage is determined by the attending physician depending on the patient’s age, the severity of anemia and research results.
A preventative dose includes taking one to five milligrams of the vitamin per day.
Aplastic anemia
Aplastic anemia is characterized by bone marrow hypoplasia and pancytopenia (decreased numbers of red blood cells, white blood cells, lymphocytes and platelets). The development of aplastic anemia occurs under the influence of external and internal factors, as well as due to qualitative and quantitative changes in stem cells and their microenvironment. Aplastic anemia can be congenital or acquired.
Causes of aplastic anemia
Aplastic anemia can develop due to:- stem cell defect;
- suppression of hematopoiesis (blood formation);
- immune reactions;
- lack of factors that stimulate hematopoiesis;
- the hematopoietic tissue does not use elements important for the body, such as iron and vitamin B12.
- hereditary factor (for example, Fanconi anemia, Diamond-Blackfan anemia);
- medications (for example, non-steroidal anti-inflammatory drugs, antibiotics, cytostatics);
- chemicals (eg, inorganic arsenic, benzene);
- viral infections (eg, parvovirus infection, human immunodeficiency virus (HIV));
- autoimmune diseases (for example, systemic lupus erythematosus);
- serious nutritional deficiencies (eg, vitamin B12, folic acid).
Symptoms of aplastic anemia
Clinical manifestations of aplastic anemia depend on the severity of pancytopenia.With aplastic anemia, the patient experiences the following symptoms:
- pallor of the skin and mucous membranes;
- headache;
- dyspnea;
- increased fatigue;
- gum bleeding (due to a decrease in the level of platelets in the blood);
- petechial rash (small red spots on the skin), bruises on the skin;
- acute or chronic infections (due to a decrease in the level of leukocytes in the blood);
- ulceration of the oropharyngeal zone (the oral mucosa, tongue, cheeks, gums and pharynx are affected);
- yellowness of the skin (a symptom of liver damage).
Diagnosis of aplastic anemia
The following changes are observed in the general blood test:- decrease in the number of red blood cells;
- decreased hemoglobin levels;
- decrease in the number of leukocytes and platelets;
- decrease in reticulocytes.
When performing a biochemical blood test, the following is observed:
- increased serum iron;
- saturation of transferrin (iron transport protein) with iron by 100%;
- increased bilirubin;
- increased lactate dehydrogenase.
- underdevelopment of all germs (erythrocyte, granulocyte, lymphocytic, monocyte and macrophage);
- replacement of bone marrow with fat (yellow bone marrow).
- ultrasound examination of parenchymal organs;
- electrocardiography (ECG) and echocardiography;
- fibrogastroduodenoscopy;
- colonoscopy;
- CT scan.
Treatment of aplastic anemia
With properly selected maintenance treatment, the condition of patients with aplastic anemia improves significantly.When treating aplastic anemia, the patient is prescribed:
- immunosuppressive drugs (for example, Cyclosporine, Methotrexate);
- glucocorticosteroids (for example, Methylprednisolone);
- antilymphocyte and antiplatelet immunoglobulins;
- antimetabolites (for example, Fludarabine);
- erythropoietin (stimulates the formation of red blood cells and stem cells).
- bone marrow transplantation (from a compatible donor);
- transfusion of blood components (erythrocytes, platelets);
- plasmapheresis (mechanical blood purification);
- compliance with the rules of asepsis and antisepsis in order to prevent the development of infection.
Depending on the effectiveness of the treatment, a patient with aplastic anemia may experience:
- complete remission (attenuation or complete disappearance of symptoms);
- partial remission;
- clinical improvement;
- lack of effect from treatment.
Treatment effectiveness | Indicators |
Complete remission |
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Partial remission |
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Clinical improvement |
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Lack of therapeutic effect |
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Hemolytic anemia
Hemolysis is the premature destruction of red blood cells. Hemolytic anemia develops when bone marrow activity is unable to compensate for the loss of red blood cells. The severity of anemia depends on whether red blood cell hemolysis began gradually or abruptly. Gradual hemolysis may be asymptomatic, while anemia with severe hemolysis can be life-threatening and cause angina pectoris, as well as cardiopulmonary decompensation. Hemolytic anemia can develop due to hereditary or acquired diseases.
According to localization, hemolysis can be:
- intracellular (for example, autoimmune hemolytic anemia);
- intravascular (for example, transfusion of incompatible blood, disseminated intravascular coagulation).
Causes of hemolytic anemia
Premature destruction of red blood cells may be due to the following reasons:- internal membrane defects of red blood cells;
- defects in the structure and synthesis of hemoglobin protein;
- enzymatic defects in the erythrocyte;
- hypersplenomegaly (increase in the size of the liver and spleen).
The following hereditary hemolytic anemias exist:
- enzymopathies (anemia in which there is a deficiency of the enzyme, deficiency of glucose-6-phosphate dehydrogenase);
- hereditary spherocytosis or Minkowski-Choffard disease (erythrocytes of irregular spherical shape);
- thalassemia (impaired synthesis of polypeptide chains included in the structure of normal hemoglobin);
- sickle cell anemia (a change in the structure of hemoglobin leads to red blood cells taking on a sickle shape).
Immune disorders are characterized by autoimmune hemolytic anemia.
Non-immune disorders can be caused by:
- pesticides (for example, pesticides, benzene);
- medications (for example, antiviral drugs, antibiotics);
- physical damage;
- infections (for example, malaria).
- defective artificial heart valve;
- disseminated intravascular coagulation;
- hemolytic uremic syndrome;
Symptoms of hemolytic anemia
Symptoms and manifestations of hemolytic anemia are varied and depend on the type of anemia, the degree of compensation, and also on what treatment the patient received.It should be noted that hemolytic anemia may be asymptomatic, and hemolysis may be detected incidentally during routine laboratory testing.
With hemolytic anemia, the following symptoms may occur:
- pallor of the skin and mucous membranes;
- brittle nails;
- tachycardia;
- increased respiratory movements;
- decreased blood pressure;
- yellowness of the skin (due to increased bilirubin levels);
- ulcers may be observed on the legs;
- skin hyperpigmentation;
- gastrointestinal manifestations (eg, abdominal pain, stool disturbances, nausea).
Prolonged hemolysis can lead to the development gallstones due to impaired bilirubin metabolism. In this case, patients may complain of abdominal pain and bronze skin color.
Diagnosis of hemolytic anemia
In a general blood test, the following is observed:- decreased hemoglobin levels;
- decreased red blood cell levels;
- increase in reticulocytes.
In a biochemical blood test, an increase in bilirubin levels is observed, as well as hemoglobinemia (an increase in free hemoglobin in the blood plasma).
Children whose mothers suffered from anemia during pregnancy also often develop iron deficiency by the first year of life.
Manifestations of anemia often include:
- feeling tired;
- sleep disorder;
- dizziness;
- nausea;
- dyspnea;
- weakness;
- brittle nails and hair, as well as hair loss;
- pale and dry skin;
- perversion of taste (for example, the desire to eat chalk, raw meat) and smell (the desire to sniff liquids with pungent odors).
It should be noted that a mild form of anemia may not manifest itself in any way, so it is very important to regularly take blood tests to determine the level of red blood cells, hemoglobin and ferritin in the blood.
During pregnancy, the normal hemoglobin level is 110 g/l or higher. A drop below normal is considered a sign of anemia.
Diet plays an important role in the treatment of anemia. Iron is absorbed from vegetables and fruits much worse than from meat products. Therefore, a pregnant woman’s diet should be rich in meat (for example, beef, liver, rabbit) and fish.
The daily requirement of iron is:
- in the first trimester of pregnancy – 15 – 18 mg;
- in the second trimester of pregnancy – 20 – 30 mg;
- in the third trimester of pregnancy – 33 – 35 mg.
Name of the drug | Active substance | Mode of application |
Sorbifer | Ferrous sulfate and ascorbic acid. | To prevent the development of anemia, you should take one tablet per day. For therapeutic purposes, you should take two tablets a day, morning and evening. |
Maltofer | Iron hydroxide. | When treating iron deficiency anemia, you should take two to three tablets ( 200 – 300 mg) per day. For prophylactic purposes, the drug is taken one tablet ( 100 mg) in a day. |
Ferretab | Ferrous fumarate and folic acid. | You must take one tablet per day; if indicated, the dosage can be increased to two to three tablets per day. |
Tardiferon | Ferrous sulfate. | For preventive purposes, take the drug starting from the fourth month of pregnancy, one tablet daily or every other day. For therapeutic purposes, you need to take two tablets a day, morning and evening. |
In addition to iron, these preparations may additionally contain ascorbic or folic acid, as well as cysteine, as they promote better absorption iron in the body. Before use, you should consult a specialist.
(or total red blood cell volume).
Note: due to absence obvious signs regeneration in peripheral blood in horses, erythrocyte characteristics are not entirely suitable for classifying anemia. A unique feature of horses is that their red blood cells remain in the bone marrow until full maturity, even with severe anemia and intense erythropoiesis. Therefore, peripheral signs of erythrocyte regeneration (reticulocytosis, macrocytosis, anisocytosis, polychromasia, Jolly bodies, nuclear erythrocytes) are almost never found in horses.
1. REGENERATIVE ANEMIA
A. Hemorrhagic anemia
Biochemical marker: Total serum protein is reduced – hypoproteinemia
1.Acute blood loss
Does not lead to a decrease in serum Fe and even leads to its increase if the bleeding is internal
Neutrphilia without shift and thrombocytosis (rare in horses)
Normocytic normochromic during the first 12-24 hours.
In dogs and cats, active erythropoiesis (macrocytosis, reticulocytosis, there may be normoblasts) occurs on days 2-3.
Destruction of large tumors (hemangiosarcomas), gastrointestinal bleeding
Thrombocytopenia below 20 thousand/µl can cause bleeding.
Coagulopathies (dicoumarol poisoning, viral and bacterial infections=>DIC syndrome)
Factor VIII deficiency - classic hemophilia (German Shepherds are predisposed)
2. Chronic blood loss
It develops slowly, clinical signs appear only with severe anemia.
Diagnosis requires a comprehensive examination of the whole body
Compensated by an adequate increase in hematopoiesis: normo/macrocytic, normochromic anemia
Not compensated by an adequate increase in hematopoiesis: hypochromic, microcytic, hypochromic iron-deficient non-regenerative anemia
B. hemolytic anemia
Caused by shortening the life of red blood cells
Often accompanied by neutrophilic leukocytosis >50 thousand (especially immune-related)
Total protein normal/increased
Jaundice varying degrees(rule out liver disease and anorexia (horses do not have a gallbladder)
How do hemolytic anemias manifest:
Intravascular hemolysis (I.G.)(lysis of circulating red blood cells): severe jaundice (increased indirect bilirubin), hemoglobinuria, increased MCH, blood in the urine. Jaundice develops within 24 hours after the onset of hemolysis. Mature neutrophilia.
Extravascular hemolysis (E.H.)(phagocytosis by the liver and spleen macrophage system): jaundice (increased direct bilirubin), no hemoglobinuria, normal MCH, no blood in urine
1. Cellular disorders (E.G.)
Pyruvate kinase deficiency(pyruvate kinase is involved in anaerobic glycolysis) in Basenjis and Beagles. Chronic anemia (normochromic, normocytic, increased reticulocytes) with crises due to illness, treatment
Occurs in the 1st year of life and subsequently leads to myelofibrosis, osteosclerosis and death at 3-5 years.
Hereditary stomatocytosis in Malamutes(low-grade macrocytic hypochromic anemia) The spleen and liver may be enlarged.
Congenital erythropoietic porphyria of cats. Synthesis of abnormal porphyrin leads to the removal of red blood cells in the spleen. The result is severe, macrocytic-hypochromic anemia.
2. Extracellular disorders (E.G. and I.G.)
The clinical picture depends on the degree and duration of the disease. Normochromic-normocytic to macrocytic anemia. The number of reticulocytes is higher than in hemorrhages. Serum Fe is normal or elevated.
For dogs, cats and horses it is of minor importance (in dogs and horses most of it is immunologically determined)
- babesiosis(I.G.) dogs
- equine piroplasmosis(Babesia caballi and Theileria equi)
- equine ehrlichiosis(Anaplasma Phagocytophila, formerly Ehrlichia equi). Granulocytopenia, thrombocytopenia, anemia. Identification of morulae in neutrophils (granulocytic ehrlichiosis).
- hemobartonosis in cats (leukemia is often mutual) I.G. and E.G.
- leptospirosis in dogs, horses (I.G.)
- INAN in horses (I.G. and E.G.) the CVS does not decrease, it even increases
- anemia with Heinz bodies(oxidation and denaturation of hemoglobin). Such red blood cells are destroyed intravascularly (I.G.) and removed in the spleen (E.G.).
As a result, horses have acute and severe anemia (causes: treatment with phenothiazine (anthelmintic), phenylhydrazine (industrial poison). High serum Fe was noted.
In dogs - raw onion poisoning, nitrites, benzocaine ointment (pain reliever), acetylphenhydrazine.
3. Chronic liver damage
Morphologically changed erythrocytes: Acanthocytes (deposition of cholesterol on the membrane).
Progressive chronic hepatitis in Bedlington Terriers. Due to a hereditary defect in copper metabolism in the Bedlington Terrier, it leads to I.G. Increased copper in plasma.
A). Copper toxicosis (storage disease) in Bedlington Terriers (hepatomegaly, lethargy, weight loss, jaundice, vomiting). The disease is inherited in an autosomal recessive manner. The normal level of copper in the blood is 75-90 mg/dl
b). Copper toxicosis also occurs in West Highlands (causes chronically progressive hepatitis)
V). Doberman Pinschers have a hereditary defect in copper accumulation in the liver with the same consequences. Bitches get sick more often than males.
- 2. Hypophosphatemia
Blood phosphorus below 0.3 mmol/l (with diabetes, severe hepatopathy, malabsorption syndrome) leads to severe hemolysis.
5. Anemia during transfusion(I.G.)
6. Isoerythrolysis of newborns
Blood type incompatibility (cats, horses)
7. Autoimmune hemolytic anemia (E.G. and I.G.).
Primary AIHA is rare.
Secondary AIHA (Ig M-mediated process)
Causes: Babesia, Anaplasma, penicillin, phenylbutazone (NSAIDs), etc.
In blood smears: spherocytes, autoagglutination of erythrocytes. The Coombs test is positive.
Note: Normoblasts can be present in the blood even in the absence of anemia.
Dogs: lead poisoning, bone marrow damage due to septicemia and endotoxic shock or after the administration of certain drugs, as well as in small quantities and for other reasons (heart pathology, hyperfunction of the adrenal cortex, inflammatory processes)
Cats: hepatic lipidosis, inflammatory processes, acute trauma.
II. NON-REGENERATIVE (aplastic) ANEMIA
Anemia due to inadequate erythropoiesis. The rate of erythrocyte maturation is less than the rate of erythrocyte destruction.
Develops slowly and reflects the lifespan of red blood cells of the animal species:
Horse: about 5 months
Dog: 3-4 months
Cat: 3-4 months
The most common type of anemia in horses. Weak or moderate, progresses for a long time, in chronic diseases
70-80% of anemia in cats, because... hematopoietic. organs are very sensitive to damage by viruses, bacteria, etc.
Total protein is normal/increased with chronic inflammation or neoplasm
There is no bilirubinemia unless there is concomitant liver damage.
A. primary disorder of erythropoiesis
Refractory (selective) anemia (only erythropoiesis is impaired, leukocytes and platelets are normal/increased)
FeLV(Fe is normal or increased, the degree of transferrin saturation tends to 100%). More than 60% of cats with anemia are positive for leukemia.
Causes of acquired aplastic anemia: bacterial, viral infections, chronic renal failure, chronic liver disease, drug effects.
In horses, cases of A.A. are rare, but have been identified with the use of phenylbutazone, the use of human erythropoietin in racehorses (Fe is increased, CVS is normal)
Total cellular destruction
Secondary to neoplastic infiltration or myelofibrosis. Loss of leukocytes, platelets and, as a consequence, thrombocytopenic hemorrhages and localized infections.
B. secondary disorder of erythropoiesis
(decreased serum Fe)
Most common in horses (mild, slowly progressive). In dogs, Fe is normal or reduced.
In cats, due to more short life erythrocytes begins faster (infections, peritonitis, pleurisy, sepsis, pyometra, cystitis)
Mainly hypochromic, microcytic
chronic renal failure(normochromic, normocytic). Some decrease in Fe and transferrin. Rarely in horses. In cats it is less common than in dogs, because In cats, erythropoietin is not produced only in the kidneys, as in dogs.
With chronic renal failure, secondary HYPERPARATHROOSIS develops, which is responsible for shortening the life of red blood cells.
Chronic liver damage. Not common in domestic animals. Fe is normal or may be elevated. OJSS is normal.
Endocrinopathies. Mild to significant anemia has been described in dogs with serious endocrinopathies (hypothyroidism, hypoadrenocorticism). Anemia is normocytic, normochromic. Serum Fe is reduced in hypothyroidism.
B. Nuclear synthesis disorders
B12 deficiency(macrocytic, normochromic) Serum Fe is increased, PVSS is normal.
Leads to disruption of DNA synthesis. The liver contains a month's supply of the vitamin, so problems begin only after a month.
In horses, the vitamin is synthesized by intestinal microflora with sufficient cobalt intake. In horses this is not a problem; the causes of anemia lie in folic acid deficiency.
In dogs, folic acid deficiency can occur due to malabsorption syndrome, chronic diarrhea, liver diseases. Pancreatic insufficiency can cause megaloblastic anemia
Folic acid antagonists: anticonvulsants (phenobarbital, etc.), cytostatics (methotrexate), trimethoprim (antibiotic).
In cats, folic acid deficiency may be caused by inadequate absorption or increased requirement.
Congenital macrocytosis of poodles. Associated with B12 deficiency (normal hematocrit, slightly reduced red blood cell count)
D. Disorders of hemoglobin synthesis
(microcytic, hypochromic)
Fe deficiency. At the latent stage, life-sustaining blood pressure increases
Fast-growing puppies/foals are more susceptible large breeds due to high demand.
Kittens grow more slowly compared to young animals of other animal species.
Iron deficiency anemia of horses and cats is normochromic, normocytic.
Leukocytes - normal or reduced, in 50-75% of cases thrombocytosis, in 30% of cases - thrombopenia (which is worse)
Sideroblastic anemias(B6 deficiency, poisons) Fe metabolism disorder.
Anemia is a condition of the body characterized by a decrease in the content of hemoglobin and red blood cells in the blood. However, anemic syndrome sometimes develops even with a normal number of red blood cells per unit volume of blood; this occurs, for example, when there is insufficient iron in animal feed, which is necessary for the synthesis of hemoglobin. Since hemoglobin is a carrier of oxygen, and red blood cells transport it, the symptom complex that develops due to oxygen deficiency is associated with this enzyme. Therefore, opinions are expressed that anemia is a decrease in the total content of only hemoglobin in the blood.
Anemia may be accompanied by general thickening of the blood; this usually occurs during intoxication, accompanied by loss of fluid in the body, but more often it is combined with oligonemia or hydremia. In these cases, the ratio between plasma and blood cells, mainly erythrocytes, changes, as evidenced by the hematocrit value.
To characterize anemia, the absolute content of hemoglobin in one red blood cell, or a color indicator that gives an idea of its relative content compared to the norm, is of great importance. Thus, anemia is hypochromic, normochromic and hyperchromic.
The concentration of hemoglobin in a cell ensures its functional activity. With a lack of respiratory enzyme in the blood, oxygen delivery to tissues is disrupted and hypoxia develops with all the ensuing consequences.
Fundamental importance in assessing the degree, type and prognosis of anemia is currently attached to the definition functional state red, i.e. active, bone marrow, when the erythroblastic germ can undergo hyperplastic, hypoplastic and even aplastic processes. Bone marrow lesions are sometimes primary in nature, affecting all hematopoiesis (with various intoxications, radiation sickness, leukemia, hereditary pathology) or one erythroid (with deficiency of B vitamins - folic acid, cobalamin and iron). Therefore, the so-called myelogenous anemia can be of hypo-, normo- and aplastic type.
An increase in the erythroblastic function of the bone marrow is a consequence of compensatory and regenerative processes and, less often, a violation of the differentiation of hematopoietic cells, for example, in human pernicious anemia, chicken erythroblastosis.
Classification of anemia. Anemia most often represents a symptom complex of the disease and less often has independent significance in human pernicidal anemia, infectious anemia of horses, sheep and goats. Consequently, a strict nosoological classification of anemia is theoretically difficult, but practically can be used for this purpose various principles: etiological, pathogenetic, histological, morphofunctional, genetic, etc. However, none of the principles can be followed to the end, since it is impossible to take into account the variety of causes of the anemic state in various diseases. Otherwise various diseases will fall into the same group. Despite the contradictory opinions, we believe that from a practical point of view, it is advisable to divide anemia according to the pathogenetic principle, which is most convenient:
1) anemia due to blood loss (posthemorrhagic);
2) anemia due to circulatory disorders (ischemic);
3) anemia due to malnutrition (nutritional);
4) anemia due to a lack of vitamins, microelements, antianemic factors (deficient);
5) anemia due to increased destruction of red blood cells (hemolytic);
6) anemia due to impaired bone marrow function (myelogenous);
7) anemia due to infectious, invasive and other diseases (functional);
8) anemia due to a violation of genetic mechanisms (hereditary).
Symptoms and pathogenesis. The main clinical signs of various anemic conditions in animals, as in humans, are the same: poor or depressed condition, pallor of the mucous membranes, shortness of breath, rapid pulse, decreased appetite, productivity, sexual potency.
Initially, the anemic state is compensated by adaptive reactions, including mobilization of the capillary and tissue pool of red blood cells, activation of bone marrow, increased blood circulation mainly due to heart contractions and ventilation of the lungs, increased activity of redox enzymes and other mechanisms. With a long and unfavorable course of the underlying disease, decompensation occurs with the development specific lesions various organs and tissues (hemosiderosis, fatty degeneration, bone marrow aplasia, etc.).
Immediately before fatal There is a disturbance in the functioning of the kidneys, liver, and central nervous system. The breakdown products of hemoglobin and bile acids (urobilin, bilirubin and other substances) appear in the urine. Bilirubin also appears in the blood, and swelling develops in various parts of the body. However, these signs vary significantly depending on the severity of anemia and the causes that caused it and, in addition, are combined with the symptoms of the underlying disease.
Diagnostics. Crucial in the diagnosis of anemia, taking into account clinical condition The animal is given to the analysis of the morphological picture of red blood, including the determination of its quantitative and qualitative indicators, including the content of hemoglobin and red blood cells. Also, an important role in establishing the nature and pathogenesis of the anemic condition is played by intravital bone marrow studies and determination of the functional state of erythrocytes, in particular resistance, life expectancy, and type of hemoglobin.
Treatment and prognosis. Treatment is most often carried out symptomatically, but if the cause of anemia is known, i.e. the underlying disease, then efforts are directed against the disease itself. For example, with extensive post-hemorrhagic anemia, blood transfusions or blood substitutes are used, saline is administered to compensate for fluid loss, and iron supplements are prescribed. For nutritional anemia, the quantitative and qualitative composition of the diet is improved, biological additives are introduced in the form of various premixes, vitamins, and iron supplements. In case of severe anemia of unknown origin, in addition, drugs that stimulate hematopoiesis are used, autohemo-, sero- and protein therapy are carried out.
The prognosis of the disease depends on the possibility of eliminating the main causes that caused anemia, the degree of its severity and the reactivity of the body.
Anemia due to blood loss (posthemorrhagic). Bleeding, leading to the development of anemia, is a consequence of a violation of the integrity of vascular wall and can be external or internal. The causes of vascular damage are quite numerous and varied, usually these are injuries and various pathological processes, including in the wall itself. Large quantities of blood are sometimes deliberately taken from large animals to obtain biological products. Depending on the rate of blood loss, acute and chronic posthemorrhagic anemia are distinguished.
Acute posthemorrhagic anemia. It develops as a result of the rapid loss of significant amounts of blood. A blood loss equal to 3% of body weight is considered life-threatening. Animals, however, have individual and species sensitivity to blood loss, and their physiological state and the presence of certain diseases. Dogs are the most sensitive to blood loss, while horses and cattle, on the contrary, tolerate blood collection in large quantities.
Pathogenesis. In the development of the main clinical manifestations of acute blood loss, the leading place is occupied by a decrease in total blood volume (hypovolemia). Loss of plasma causes fall blood pressure and the development of collapse. A decrease in the number of circulating red blood cells leads to hypoxia, to which the central nervous system is most sensitive. Hypoxia stimulates the production of erythropoietin, the latter, in turn, enhances ernthropoiesis in the bone marrow, due to which the content of red blood cells in the blood is gradually restored, and then the general condition is normalized.
Clinic and blood picture. Acute blood loss is characterized primarily by symptoms of collapse: adynamia, severe weakness, cold sweat, vomiting, depression, rapid thready pulse, a sharp drop in blood pressure, cyanosis, decreased body temperature, convulsions. In the case of a favorable outcome, these symptoms are replaced by the development of anemia syndrome itself. Directly during bleeding, a gradual decrease in the content of red blood cells and hemoglobin occurs in the blood, as well as a sharp decrease in platelets as a result of the formation of blood clots. After bleeding has stopped, the content of red blood cells and, therefore, hemoglobin may increase slightly due to the release of cells from the depot (especially the spleen) and a decrease in the vascular bed due to contraction of capillaries. Therefore, the degree of anemia is an imprecise indicator of the amount of blood lost.
In the first days after bleeding, a further decrease in the number of red blood cells and hemoglobin content occurs, mainly due to hydremia, which develops as a result of fluid entering the blood from tissues. In the blood, oligochromemia and oligocythemia are noted with a color indicator below one, a sharp decrease in hematocrit. A few days later, young forms of erythrocytes - reticulocytes, polychrome erythrocytes, normoblasts - are found in the blood of some animal species (dogs, pigs, etc.), which indicates the revival of erythropoiesis in the bone marrow. In the morphology of erythrocytes, poikilocytosis and anisocytosis with a predominance of microcytes are noted.
When examining bone marrow punctates, increased cellularity is observed with a large number of oxyphilic erythroblasts, the so-called red bone marrow, the predominance of the erythroblastic germ over the granulocytic one, but the latter is often also somewhat hyperplastic. Therefore, simultaneously with the regenerative forms of erythrocytes, young cells of the granulocytic series (band neutrophils, metamyelocytes) appear in the blood with an increase in the total number of leukocytes. The highest leukocytosis occurs with internal bleeding.
According to some authors, two phases can be distinguished in the change in the picture of white blood during acute blood loss: the initial one with leukopenia and lymphocytosis and the subsequent one with leukocytosis and neutrophilia. Biochemical and biophysical changes in the composition and properties of blood are characterized by an acceleration of clotting time, an increase in ROE and, mainly, a change in the level of iron in plasma. With sufficient reserves of iron in the depot, its level in the plasma quickly recovers after a sharp decrease, and on the contrary, with depletion, a picture of chronic iron deficiency anemia develops.
The diagnosis of acute posthemorrhagic anemia is not difficult if the cause of external blood loss is known. In internal hemorrhage, the location and cause are difficult to determine and the diagnosis should be based on clinical signs and findings laboratory tests.
Treatment of acute posthemorrhagic anemia consists of stopping bleeding, using antishock drugs, blood transfusion of whole blood or its components and substitutes, as well as stimulating hematopoiesis with the administration of iron supplements, and improving nutrition. In farm and domestic animals, it is most effective to simply stop bleeding, intravenously administer a large amount of saline or specific blood serum, use cardiovascular drugs and iron supplements, and improve the quality of feeding.
Chronic posthemorrhagic anemia. This disease occurs as a result of small but prolonged blood loss, usually internal, or is a consequence of acute blood loss due to iron deficiency in the body or functional bone marrow failure. The causes of internal blood loss, as mentioned above, are very diverse, and they cannot always be established during life. In farm and domestic animals, internal bleeding is most often observed due to ulcers. digestive tract(dogs, pigs), perforation of the walls of the stomach or intestines by foreign bodies (dogs, large and small cattle), tumors of the reproductive apparatus (dogs, horses), parasitic diseases (horses, cattle).
In the pathogenesis of chronic posthemorrhagic anemia, iron deficiency plays a major role, leading to hypofunction of erythropoietic activity of the bone marrow and the gradual development of hypoxia with resulting adverse consequences.
Clinic and blood picture. Animals experience lethargy, decreased performance and productivity, pale mucous membranes, swelling of the extremities, and heart murmurs. The blood picture is characterized by hypochromic anemia with a sharp decrease in the color index. Degenerative changes in erythrocytes prevail over regenerative ones: poikilocytosis, anisocytosis, anisochromia. The platelet count is usually elevated. The condition of the bone marrow depends on the duration of anemia. In the initial period, there is an increase in its erythropoietic function with the production of normal red blood cells, and in the future one can see a violation of the maturation of red blood cells as a result of insufficient hemoglobinization of red blood cells. These functional disorders of hematopoiesis are reversible and indicate a hyporegenerative state of the bone marrow. The outcome of chronic posthemorrhagic anemia in the hyporegenerative stage indicates the unresponsiveness of the body.
Treatment of chronic posthemorrhagic anemia is more complex than acute one. Due to the difficulty or ability to find and eliminate the underlying disease causing chronic anemia, treatment is often symptomatic and aimed at restoring constantly consumed iron in the body and stimulating erythropoiesis. For this purpose, various iron preparations or foods with a high iron content are introduced into the diet, vitamin preparations that stimulate erythropoiesis are prescribed, and sometimes, in case of severe anemia, blood transfusions are resorted to. The most acceptable options for animals are also the administration of iron supplements and improved feeding with various vitamin supplements. It should be borne in mind that with severe anemia, the animal may die or sharply reduce productivity, so further treatment is not always advisable.
Anemia due to circulatory disorders (ischemic). Ischemia develops when there is a local circulatory disorder due to the closure of the lumen of the vessel as a result of its mechanical compression, blockage (thrombus, parasites), damage to the vessel walls or the vasomotor action of a number of substances and factors. In animals, ischemia usually occurs when a bandage or tourniquet is too tight, exposure to low temperatures (lying on a cement floor in winter), mechanical pressure from large objects during accidents in livestock buildings or natural disasters. Anemic parts of the body or tissue are pale, the temperature is low, and pain sensitivity is almost absent. If the causes are not eliminated, then dystrophic and atrophic changes may develop in the anemic tissue due to oxygen starvation, lack of nutrients, and impaired thermoregulation. However, if there are collateral pathways in the body, blood circulation in anemic tissue can be restored very quickly and irreversible damage will not occur.
Treatment consists primarily of eliminating the underlying cause that caused ischemia and using symptomatic therapy. If the cause is unknown or difficult and impossible to eliminate, treatment is ineffective.
Anemia is deficient. Deficiency anemias develop with insufficient intake or use of certain substances (vitamins, microelements, antianemic factors, etc.). In most cases, anemia due to nutritional or metabolic disorders, and less often due to infectious, invasive and other diseases, are also deficient in nature. Chronic posthemorrhagic anemia ultimately leads to iron deficiency.
In first place in terms of frequency and significance for animals, as well as for humans, are iron deficiency anemia.
Anemia due to iron deficiency. The group of iron deficiency anemia includes anemia of different etiologies, but with a single symptom - lack of iron in the body (mainly in the blood serum, bone marrow, depot). With iron deficiency, hemoglobin formation is disrupted, hypochromic anemia and trophic changes in tissues occur due to hypoxia, leading to disruption of redox processes. The reasons for the development of deficiency are varied, but the main one is insufficient intake and poor use or large loss of iron. In farm animals, it mainly comes from feed and milk, so malnutrition contributes to the development of iron deficiency. It is especially often observed in young animals. In calves and foals, insufficient maternal iron stores lead to the development of neonatal anemia. In the future, it intensifies when switching to feeding with low-quality roughage.
Iron deficiency anemia poses a particular problem for pig farming in connection with the transition to an industrial basis. Keeping pigs on a cement base deprived them of the ability to replenish their iron stores by eating clay. It has now been established that iron can be absorbed not only in the form of complex organic compounds, but also in simpler compounds. Important in the absorption of iron has a condition in the gastrointestinal tract. Achylia and inflammatory processes in the stomach (gastritis, ulcers) reduce its absorption. Hereditary and other changes in the transferrin system can disrupt the delivery of iron to the site of hemoglobin formation. Its increased consumption in animals occurs during constant and high lactation, increased exploitation, intensive growth of young animals, various blood losses, including when collecting blood for tests and the manufacture of biological products, as well as various diseases (porcine ulcer disease, chronic hematuria of large cattle, equine opistarchosis and other diseases).
Clinic and blood picture. The clinical picture of iron deficiency anemia consists of signs characteristic of many anemias and symptoms of tissue iron deficiency. Animals experience lethargy, pale mucous membranes, shortness of breath, tachycardia, they lag behind in growth and development, productivity often decreases, and periodic gastrointestinal disorders, sometimes there are perversions of appetite when eating food that is not typical for them, hair loss occurs or, conversely, a delay in molting, and the growth of hooves and horns is disrupted.
A blood test reveals more or less severe anemia of a hypochromic nature. The color index is usually well below one. There is a distinct hypochromia of erythrocytes, when they are pale in color with a large light zone in the center, anisocytosis, and poikilocytosis. The content of reticulocytes and polychromatophils is normal or slightly increased. The platelet count is also normal or slightly elevated if there is chronic bleeding. ESR was slightly accelerated. In some animals, for example in large and small cattle, ESR is not expressed, and in the blood there are usually no reticulocytes or very few of them, even in recovery period with large blood losses. In the bone marrow, there is irritation of the red germ, a predominance of immature basophilic and polychrome erythroblasts over oxyphilic ones, the so-called “blue” bone marrow with a normal number of mitoses. The number of sideroblasts is usually reduced. This phenomenon indicates a delay in the maturation of red blood cells as a result of insufficient hemoglobinization.
Diagnosis of iron deficiency anemia is not difficult. First of all, clinical symptoms, blood tests and the results of determining non-hemoglobin iron are taken into account. Treatment is quite effective and boils down to prescribing iron supplements, improving feeding, living conditions and operation.
Anemia due to deficiency of vitamins B12 (cobalamin) and B6 (folic acid). As a result of a lack of these substances, people experience pernicious pernicious anemia or Addison-Beerman disease, the clinical syndrome of which is characterized by damage to the hematopoietic tissue, digestive and nervous systems. The reasons for the deficiency of these vitamins, like iron, are also varied and are determined by the same factors: insufficient intake, impaired absorption, use, increased consumption. Since food or feed rich in these vitamins is usually consumed, and only artificial restriction can create a deficiency in intake. Violation of absorption processes and increased consumption are of greater importance in the development of these vitamin deficiencies. In addition, for the absorption of vitamin B12, it is necessary to form a complex with a special glycoprotein (internal Castle factor), which is produced in the stomach, and the complex itself is absorbed in the small intestine. Violation of the absorption of vitamin B12 also leads to a violation of the production of internal factor, which can be hereditary or is a consequence of stomach disease (achylia, hypo- and anacid gastritis) and other disorders of the digestive system ( chronic enteritis). An increased consumption of vitamins is observed during pregnancy and helminthic infestation (broad tapeworm, bovine tapeworm), and dysbacteriosis.
The blood picture with a deficiency of vitamins B12 and B6 is characterized by hyperchromic anemia, leukopenia (due to neutrophils), thrombocytopenia. Red blood cells in pernicious anemia are large, large, without central clearing, resembling primary embryonic megalocyte cells. They often contain remnants of the nucleus (Joles bodies, Cabot rings), and oxyphilic erythroblasts are found.
In the bone marrow, irritated red germ and megaloblasts are found. Megaloblasts are characterized by big sizes, a delicate structure of the nucleus that often undergoes degenerative changes (karyorrhexis). Asynchronous maturation of the nucleus and cytoplasm is noted, when the nucleus is young, loose, and the cytoplasm is already oxyphilic, i.e., has undergone hemoglobinization. Changes in myeloid cells are also significant. They are increased in size, there are very large myelocytes, megamyelocytes, band and segmented neutrophils, the latter are often hypersegmented. Changes in hematopoiesis are more pronounced with vitamin B12 deficiency than with folate deficiency.
In farm and domestic animals, similar changes rarely occur; there are isolated cases of descriptions of diseases similar to malignant anemia. It is likely that animals are less likely to experience a deficiency of these substances; in addition, in some species (cattle and small cattle, horses) they are synthesized in large quantities by microorganisms in the forestomach and large intestine. Only in certain diseases (gastric achylia, helminthic infestation, toxic liver dystrophy, tumors, etc.) does hypochromic anemia with macrocytosis of erythrocytes, anisocytosis, and poikilocytosis develop in the blood. The number of leukocytes is usually normal or increased due to neutrophils with a slight regenerative shift.
In animals, prevention and treatment of all phases of pernicious anemia, as well as other deficiency conditions, comes down to improving feeding, maintenance, and the use of appropriate vitamins and microelements (cobalt, selenium).
In the presence of other diseases (gastrointestinal, liver, invasive), specific or pathogenetic therapy is carried out.
Anemia due to the destruction of red blood cells (hemolytic). Hemolytic anemias represent a large group of pathological conditions, united by the common feature of increased destruction of red blood cells and erythroblasts. Destruction can occur inside the vessels, i.e. in the blood, by disrupting the integrity of the cell membrane with the release of hemoglobin (hemolysis), or intracellularly, in tissues, especially the spleen, as a result of changes in the plasticity of the erythrocyte (sequestration, erythrocytolysis). The destruction of erythroblasts in the bone marrow indicates the ineffectiveness of erythropoiesis. In all these cases, the lifespan of the cell is reduced. Consequently, a slightly different definition of the concept of “hemolytic anemia” is possible - this is anemia with a shortened life span of red blood cells.
According to modern concepts, the destruction of erythrocytes is caused either by congenital disorders of cytomembrane structures, including hereditary abnormalities in the content and structure of enzymes and hemoglobin (enzyme- and hemoglobinopathies), or by the direct effect of toxic hemolytic factors on the blood and bone marrow. The latter can be divided into numerous physical (high and low temperature, hyperoxia, ionizing radiation), chemical (chemical elements, simple and complex organic and inorganic compounds, including dyes, herbicides, insecticides, drugs), biological (various antigens, parasites, bacteria and viruses, various toxins of plants, insects, reptiles) and other factors.
In animals, hereditary anomalies leading to the development of hemolytic anemia have not yet been sufficiently studied and only a few such conditions have been described (paralytic hemoglobinemia of horses, postpartum and chronic hemoglobinuria of cattle), and their genetic cause has not yet been precisely established. In contrast, there is extensive information about the effect of hemolytic factors on the blood of animals. They relate primarily to protozoal and invasive diseases, poisoning with pesticides and other inorganic and organic compounds, the effects of sudden low and high temperatures (frostbite, burns), ionizing radiation (radio damage), as well as the effects of medicinal and biological drugs(vaccines, serums, premixes).
The group of hemolytic anemias, regardless of the causes that caused them, is characterized by many common clinical signs, which are determined by the destruction of red blood cells and breakdown products, primarily hemoglobin. With acute breakdown of red blood cells (hemolytic crisis), in addition to a pronounced anemia syndrome of usually normochromic nature, hemoglobinuria and hemosideuria develop.
Hemoglobinemia in animals is observed in protozoal diseases (pyroplasmosis, anaplasmosis, trypanosomosis, etc.), in which parasites destroy red blood cells directly and with their toxins. Hemoglobinemia often occurs under the influence of chemical substances, used for medicinal purposes (potassium chloride, creolin, antifibrin, phenacetin, etc.). Less commonly, hemoglobinemia develops in acute infectious diseases(horse influenza, carnivore distemper), with severe burns and cooling of the body. Hemoglobinemia is caused by intravenous administration of incompatible blood and various serums containing iso- and heterolysins. In horses, when tetanus serum is administered, a typical hemolytic crisis develops, but the blood picture quickly normalizes. In a hemolytic crisis, a pronounced fever of a relapsing type is usually observed, and in a chronic decay, the temperature is subfibrile or almost normal and the condition of the animals is relatively satisfactory. Simultaneously with the development of the underlying disease that causes hemolytic anemia, animals experience cardiac weakness, shortness of breath, and decreased performance and productivity.
Diagnosis of hemolytic anemia itself is based on the clinical picture (jaundice, enlarged liver, spleen, cardiac and respiratory disorders) and mainly on laboratory tests of blood (content of red blood cells, their shape and size, presence of inclusions, hemoglobin level), urine and feces ( for bilirubin).
It is more difficult to determine the etiopathogenesis of the condition, especially in cases of its genetic or autoimmune origin.
Treatment is usually aimed at the underlying disease using specific therapies. Sometimes intervention is not required if the underlying cause of the anemic condition can be eliminated, or if it is necessary to apply symptomatic treatment with improved feeding, living conditions and operation.
What is this?
Immune-mediated (autoimmune) hemolytic anemia (AIHA) is a condition where the body's immune system attacks its own red blood cells.
The part of the immune system that produces antibodies begins to direct them against the body's own red blood cells.
Antibody proteins are attached to red blood cells - markers for destruction. When destroyed large quantity red blood cells indicate the development of anemia, the patient feels sick and weak. Since red blood cells are destroyed in the body, the patient develops jaundice rather than pale skin and mucous membranes.
Removing old blood cells and recycling their components is normal
Red blood cells have a specific duration life cycle from the moment it leaves the bone marrow until the end of life as an oxygen carrier, when the cells become too dense to pass through the thin capillaries.
Red blood cells must be sufficiently pliable and plastic to participate in the transport of oxygen and carbon dioxide, and when the cells become functionally unusable, the body recycles (destroys) them and reuses their components.
Disease
When the immune system flags too many cells for removal, problems begin.
The spleen increases in size due to the need to synthesize more cells.
The liver cannot cope with the huge amount of bilirubin and the patient becomes icteric, which is manifested by a yellow or orange coloration of the tissues.
Massive destruction of innocent red blood cells occurs, this process is called intravascular hemolysis.
Ultimately, there is a lack of red blood cells in the bloodstream, insufficient oxygen supply to tissues and removal of metabolic products.
The situation is getting critical life threatening patient.
Signs of the disease that can be seen at home
The animal exhibits severe weakness, lack of activity, and lack of interest in food.
The urine may be dark orange or even brown.
The color of visible mucous membranes and conjunctiva is pale or yellow.
Fever may occur.
Diagnostics
Part of the clinical examination includes blood tests.
With severe hemolysis, a decrease in the content of red blood cells, a decrease in hematocrit, a yellow or orange coloration of the blood serum, and an increase in bilirubin in a biochemical blood test are usually detected.
Anemia is a condition in which the content of functional red cells (erythrocytes) in the blood is reduced. Anemia can be mild or severe and may be due to bleeding, red blood cell destruction (RAC), or insufficient red blood cell production. If anemia is detected, it is necessary to find out the cause.
Research to detect regenerative anemia
Anemia that develops due to insufficient production of red blood cells in the bone marrow is called regenerative anemia.
The cause of such anemia is chronic inflammatory diseases(chronic diseases of the skin, teeth and others), kidney failure, various types of cancer or certain drugs (especially chemotherapy).
Normally, when red blood cells are lost, oxygen levels in the blood decrease, which stimulates the bone marrow to produce red blood cells. These types of anemia are called “regenerative” because the bone marrow responds by increasing the production of red blood cells.
With bleeding and autoimmune destruction of red blood cells, regenerative anemia is also observed. Several ways have been developed to determine the type of anemia (whether it is regenerative or not).
The laboratory produces complete clinical analysis blood, examining the number of red blood cells and white blood cells, their size, shape, maturity, and ratios. A patient with regenerative anemia has very active bone marrow. Red blood cells enter the bloodstream not mature enough, so they can differ in size and pigment brightness (less mature red blood cells are larger and paler than mature cells).
Moreover, the precursors of erythrocytes, reticulocytes, can enter the bloodstream (they are so immature that they cannot be called erythrocytes).
When the bone marrow is very strongly stimulated, red blood cells with a cell nucleus can be released into the bloodstream. These indicators indicate regenerative anemia. This means that red blood cells are lost during bleeding, hemorrhage or during active work the immune system destroys its own blood cells.
Studies revealing autoimmune destruction
When examining blood, there are several indicators that can determine the destruction of red blood cells or blood loss. You might think that blood loss is easy to detect, but internal hemorrhages occur that are difficult to detect.
Jaundice
Jaundice is the yellow coloration of animal tissues when the liver cannot cope with large amounts of bilirubin (iron-containing pigment formed when red blood cells are destroyed) supplied to it with the blood.
Normally, red blood cells are removed from the bloodstream as cells age and lose plasticity. The iron in red blood cells is used again in the liver.
When a large number of red blood cells are destroyed, the liver does not have time to utilize all the pigment, and it spreads throughout the body, turning the urine, gums and whites of the eyes yellow-orange.
Can jaundice only be caused by autoimmune destruction of red blood cells? Of course not. Liver failure leads to jaundice when the diseased liver is unable to process normal amounts of bilirubin.
Typically, regenerative anemia with jaundice indicates autoimmune destruction of red blood cells.
Spherocytes
Spherocytes are spherical red blood cells that are found in the blood when the spleen does not completely remove old red blood cells from the bloodstream.
The spleen cells “bite off” part of the red blood cell, and it goes on to circulate in the blood. A normal red blood cell is biconcave and disc-shaped, the center of the cell is paler than the peripheral part. After the loss of part of the cell, the red blood cell acquires a spherical shape and becomes darker in color. The presence of spherocytes indicates the process of destruction of red blood cells.
Autoagglutination
In acute cases of AIHA, the autoimmune destruction of red blood cells is so severe that they clump together (as their membranes with attached antibodies stick to each other) when a drop of blood is placed on a glass slide under a microscope. The picture appears as follows: a yellow spot with a small red lump in the center. This sign is very unfavorable.
Leukemoid reaction
In the classic case of AIHA, the bone marrow response is so strong that white blood cells also undergo changes, since they are also produced in the bone marrow. The number of leukocytes in the blood increases significantly.
Additional Research
Coombs test (direct antibody test)
The Coombs test is designed to detect antibodies on red blood cells and is a classic reaction for detecting AIHA.
Unfortunately, the test results are not clear. It can be a false positive in the presence of inflammation or infection (resulting in antibodies attaching to the lining of red blood cells), or after a blood transfusion (ultimately the foreign cells are eliminated by the immune system).
Also, the Coombs test may be falsely negative due to various reasons.
If the clinical picture of the disease coincides with AIHA, the Coombs test is often not performed. Remember, the causes of hemolysis (destruction of red blood cells) are not always associated with immune reactions. Onions in large quantities (it is assumed that garlic too) can cause hemolysis in dogs.
Zinc poisoning, such as from licking zinc oxide ointment from the skin, can lead to hemolysis.
In young animals, a genetically determined deformation of erythrocytes can be suspected.
Treatment and observation during a crisis
Patients with AIHA are often unstable.
If the hematocrit is critically low, a blood transfusion may be required. At acute form The course of the disease may require multiple blood transfusions.
General supportive care includes maintaining fluid balance and providing the body with essential nutrients.
It is most important to stop hemolysis by suppressing the destructive effect of the immune system on red blood cells.
Blood transfusion
Transfusion of whole donor blood can save a patient with a critically low hematocrit. However, it is necessary to remember: the problem is that the immune system destroys its own cells, then what is the chance of preserving foreign cells?
A good red cell compatibility is ideal, but due to the increased immune response, the outcome of the transfusion may be different. Therefore, multiple blood transfusions should not be performed.
Immune suppression
Corticosteroid hormones in high doses have an immunosuppressive effect. Prednisolone And dexamethasone are most often used for this purpose.
These hormones have a direct toxic effect on lymphocytes - cells that synthesize antibodies. If red blood cells are not bound by antibodies, they are not removed by the immune system, so stopping antibody production is important part treatment of AIHA.
These hormones inhibit the activity of reticuloendothelial cells that remove antibody-labeled blood cells.
Corticosteroids are usually sufficient to suppress the immune system. The problem is that if they are stopped early, hemolysis will begin again. You will likely need to take the hormones for weeks, even months, before tapering.
The medications are taken under the control of the blood picture. Expect the animal to be on steroid therapy for about 4 months, many will require ongoing low doses to prevent relapse.
Corticosteroids in high doses cause thirst, redistribution of body fat, thinning of the skin, shortness of breath, predisposition to diseases of the urinary system and other signs characteristic of Cushing's syndrome. Such side effects accompany long-term use of corticosteroids, but in the case of AIHA there is often no other choice.
It is important to remember that side effects decrease with decreasing dosage of drugs.
More severe immune suppression
If there is no desired effect on the administration of corticosteroids, additional immunosuppressants are necessary. In this case it is often used azathioprim And cyclophosphamide, they are very strong drugs.
Cyclosporine is an immunomodulator, popular in transplantology.
Its advantage is that it does not suppress bone marrow function. It was used as a promising additional drug for AIHA, but 2 significant drawbacks emerged: high cost and blood monitoring to control the correct dose of the drug. The cost of treatment is very high, but the results can be very good.
Why did this disease affect your animal?
When something serious happens, you always want to know why.
Unfortunately, if the patient is a dog, then this question will be difficult to answer.
Research results show that in 60-75% of cases the exact cause cannot be identified.
In some cases, the cause can be found: a factor provoking the reaction. Some medications can cause a reaction that stimulates the immune system and masquerades as red blood cell proteins. The immune system monitors not only proteins similar to the drug, but also red blood cells with a similar protein. Such drugs are penicillin, trimethoprim sulfa and methimazole.
Some breeds are predisposed to developing AIHA: Cocker Spaniel, Poodle, Old English Sheepdog, Irish Setter.
Complications of AIHA
Thromboembolism
This disease is the leading cause of death in dogs with AIHA (30-80% of dogs dying from AIHA have this disease).
A large blood clot is called blood clot, blocking a blood vessel. The vessel is called thrombosed. Embolism is the process when small parts break off from a blood clot and spread throughout the body. These mini blood clots clog smaller vessels, leading to poor circulation. In areas of blockage, an inflammatory reaction occurs that dissolves the clots; it can become health threatening when many vessels are affected.
AIHA is relatively rare, but very serious illness With high level mortality. Unfortunately, many dogs die.
