Autoimmune hemolytic anemia in dogs. Causes of anemia in cats. Additional examinations of cats with anemia
Anemia – pathological condition, characterized by a decrease in hemoglobin content, a decrease in hematocrit and the number of red blood cells per unit volume of blood.
Anemia aplastic- a disease caused by inhibition of the hematopoietic function of the bone marrow.
The mechanism of development of aplastic anemia is probably associated with immune processes. The disease can be caused or exacerbated by hormonal imbalances, bone marrow damage, or a genetic predisposition.
Drowsiness, pallor, petechial hemorrhages or bleeding of mucous membranes, hematuria, hemoptysis, melena due to thrombocytopenia, periodic fever, frequent or prolonged inflammatory processes of leukopenia are characteristic.
Diagnostics
Aplastic anemia is differentiated from infection and intoxication, as well as proliferative and infiltrative processes in the bone marrow.
Tests are used for pancytopenia (ehrlichiosis, feline leukemia virus), for antibodies to erythrocytes (Coombs test), leukocytes and platelets, for other autoimmune diseases (antinuclear antibodies to systemic lupus erythematosus). Bone marrow aspiration biopsy may reveal an insufficient number of hematopoietic elements and a significant amount of fat.
Treatment
Antibiotic therapy, blood or platelet transfusion, glucocorticoids and other immunosuppressants, anabolic steroids and colony-stimulating factors are prescribed separately or in combination.
With the appearance of drowsiness, fever and hemorrhages that occur with a relapse of anemia, leukopenia and thrombocytopenia, you should immediately consult a doctor. It is necessary to palpate the lymph nodes daily, measure body temperature. Recovery may take 1 or more months depending on the results of the CBC (degree of decrease in the number of blood cells and platelets), age and general condition animal, as well as the cause of the disease.
Anemia autoimmune hemolytic
Anemia caused by the destruction of erythrocytes by autoantibodies, followed by their capture by macrophages and deposition in the spleen.
Specific autoantibodies are produced against membrane antigens of unchanged (primary autoimmune hemolytic anemia) or damaged (secondary autoimmune hemolytic anemia) red blood cells.
In autoimmune hemolytic anemia, the hematopoietic, lymphatic, and immune systems are affected. If the liver and biliary tract cannot cope with the bilirubin load, hyperbilirubinemia and jaundice develop.
Hypoxia can lead to centrilobular necrosis of the liver. Also, hypoxia causes tachycardia, and a decrease in the viscosity and turbulence of blood flow causes muffled heart tones. At chronic anemia heart failure develops against the background of high cardiac output. From the side respiratory system tachypnea is observed, from the side of the kidneys and renal pathways - necrosis of the renal tubules.
In the anamnesis, episodes of loss of consciousness, lethargy, drowsiness, loss of appetite, shortness of breath, rapid breathing sometimes polyuria and polydipsia.
During the examination, attention is drawn to the pallor of the mucous membranes, tachycardia, tachypnea, jaundice, dark urine stained with hemoglobin or bilirubin), fever, enlargement of the spleen, liver and lymph nodes, systolic murmur, gallop rhythm. With concomitant thrombocytopenia in the syndrome of disseminated vascular coagulation, petechiae, ecchymosis or melena may be observed.
Diagnostics
A general clinical blood test reveals: anemia, increased average volume erythrocytes (3-5 days after the hemolytic crisis), shift of the leukocyte formula to the left. Urine contains hemoglobin.
In the bone marrow punctate, hyperplasia of the erythroid process is usually determined, with regenerative anemia, maturation stops and cytopenia of young cells is observed, and with chronic form- myelofibrosis.
Physical examination reveals hepatosplenomegaly, reactive lymph node enlargement, signs of congestive heart failure (cardiomegaly, nutmeg), thromboembolism pulmonary artery syndrome of disseminated intravascular coagulation.
Treatment
In acute hemolytic crisis, treatment is carried out in a hospital, until hematocrit stabilizes, hemolysis ceases and anemia is eliminated. With the development of complications (syndrome of disseminated intravascular coagulation, pulmonary embolism, thrombocytopenia, gastrointestinal bleeding, heart failure), if necessary, repeated blood transfusions are indicated for hospitalization. Chronic extravascular hemolysis of a mild degree of hospitalization does not require hospitalization if anemia is not clinically manifested.
It should be understood that autoimmune hemolytic anemia and its complications are life-threatening, and lifelong therapy may be required, in some cases accompanied by severe adverse reactions, and that the disease may recur.
When choosing drug and infusion therapy that caused the disease (infection, drugs for secondary autoimmune hemolytic anemia). Prednisolone is prescribed, if there is no effect, immunosuppressants are prescribed.
IN acute phase autoimmune hemolytic anemia, hematocrit should be measured daily to assess the effectiveness of therapy and the need for blood transfusion. In the hospital, several times a day, the respiratory rate and heart rate are counted, general and biochemical blood tests are performed. X-rays are often taken if pulmonary embolism is suspected. chest and study of arterial blood gases.
During the first month outpatient treatment until the condition stabilizes, hematocrit is examined once a week, then every 2 weeks for 2 months
Anemia hemolytic Heinz (Ehrlich)
Anemia due to the penetration of oxidants into the body and the destruction of hemoglobin.
Fragments of the latter, found in erythrocytes, called Heinz (Ehrlich) bodies, or inclusions.
Defective red blood cells are deposited or lysed in the spleen. In some cases, the disease is accompanied by methemoglobinemia.
It is more often observed in cats, whose hemoglobin is more sensitive to the action of oxidants. Onions, substances containing zinc, D, I, L-methionine (in cats) have oxidizing properties; as well as drugs - acetaminophen (in cats) and phenacetin (in dogs)
Diagnostics
In severe anemia, free hemoglobin is determined in the blood and urine. Hematocrit and reticulocyte count indicate the severity of regenerative anemia.
Treatment
It is enough to exclude the traumatic factor - oxidants, and carry out symptomatic therapy (blood transfusion, oxygen therapy, activity restriction).
The hematocrit, reticulocyte count, and percentage of red blood cells containing Heinz bodies should be periodically examined, documenting the disappearance of the latter and the restoration of the number of normal red blood cells. If it was possible to overcome the hemolysis of erythrocytes, the prognosis is favorable.
Iron deficiency anemia
A pathological condition caused by iron deficiency in the body.
With insufficient intake of this element, the erythropoietic function of the bone marrow is disturbed. The most common reason iron deficiency anemia- blood loss, the source of which is most often the gastrointestinal tract, less often urinary tract. The cause of anemia can be neoplasms, severe flea damage, as well as nematode invasion.
Iron deficiency anemia is more common in dogs and less common in adult cats. In 50% of 5-10-week-old kittens, so-called transient iron deficiency anemia of the newborn develops.
Diagnostics
Microcytosis is found in the blood, hypochromia is a characteristic sign. Low plasma iron levels confirm the diagnosis.
Treatment
Replenishment of iron reserves - ferrum-lek is used for parenteral administration. Every 1-4 weeks it is necessary to control the hemogram. In some animals, recovery normal recovery the normal formula of red blood cells can occur within a few months.
Anemia hypoplastic macrocytic
A hereditary disease characterized by a stop in the development of the nucleus in the cell of the precursor of the erythrocyte due to a violation of DNA synthesis during the normal development of the cytoplasm.
Several factors have been identified that predispose to macrocytic anemia or provoke it:
Unbalanced nutrition (lack of folic acid, vitamin B12 deficiency)
Toxins (dilantin intoxication, methotrexate poisoning or other toxic substances)
Ancestral (toy poodle)
Macrocytic anemia is usually mild
Diagnostics
Classical macrocytic anemia (large average volume of erythrocytes) and concomitant normochromia (average hemoglobin concentration.
Of specific studies, tests for the detection of feline leukemia virus and immunodeficiency are important: retroviral infection is the most common cause of megaloblastic anemia in cats. The final diagnosis is based on bone marrow examination, often in all cell lines.
Treatment
Aimed at eliminating the cause of the disease. The effectiveness of treatment is determined by the results of a complete blood count (weekly) and bone marrow (individually).
In cats with positive reaction for the leukemia virus, the prognosis is cautious. In animals with drug-induced anemia, the prognosis is favorable if the drug is stopped in a timely manner.
Anemia in chronic kidney disease (progressive kidney failure)
It is characterized by low hematocrit, a decrease in the number of erythrocytes and the content of hemoglobin in them, and hypoplasia of erythroid elements of the bone marrow.
The cause of anemia can be congenital and acquired forms of renal failure (pyelonephritis, glomerulonephritis, amyloidosis)
Diagnostics
In clinical and biochemical analyzes of blood and urine, normocytic normochromic regenerator anemia, high levels of blood urea nitrogen, createnin, phosphorus, calcium, low bicarbonate and potassium are released. There are violations of urination, moderate proteinuria, the presence of active sediment. On radiographs, small, irregularly shaped kidneys with a disturbed structure are visible.
Treatment
If symptoms of anemia appear, it is necessary to increase the number of red blood cells. Erythropoietin is used to correct anemia in chronic renal failure. For the treatment of ulcers and bleeding of the gastrointestinal tract - ranitidine, sucralfate. Systemic hypertension should also be treated.
Determination of hematocrit is carried out in the first 3 months weekly, then 1 time in 1-2 months, arterial pressure measured 1-2 times a month.
Sourced from www.icatcare.org
Anemia is a disease in which the number of red blood cells (erythrocytes) decreases in the blood. In severe anemia, a cat's gums become very pale.
Red blood cells are a special type of cell containing hemoglobin, a special molecule containing iron that can efficiently bind oxygen. In the process of breathing, oxygen enters the lungs with air, where it is absorbed by the blood, binding to the hemoglobin of red blood cells. As blood circulates through the body, hemoglobin transfers oxygen to the body's tissues, which is vital for maintaining health. It is the hemoglobin in red blood cells that gives blood its characteristic red color.
If a cat is anemic, the ability of red blood cells to absorb oxygen from the air and deliver it to body tissues is reduced. This can lead to many problems, but most often manifests itself in the form of weakness and lethargy. In severe cases, anemia manifests itself in rapid breathing, shortness of breath. This is because the cat is trying to move more air through the lungs in order to increase the level of oxygen in the blood.
Without proper treatment, anemia becomes a debilitating disease and, in severe cases, can be life-threatening. Unfortunately, cats are often prone to developing anemia. This is partly due to the fact that their red blood cells have a relatively short lifespan of approximately 70 days. And, for example, in dogs and people about 110-120 days. This means that cats have a faster turnover of red blood cells, and if left untreated, the disease can progress quite quickly.
In addition, anemia can develop due to various diseases and infections.
Types of anemia in cats
By and large, anemia exists in two forms - regenerative and non-regenerative. In the regenerative form of the disease, the bone marrow responds by trying to increase the production of red blood cells to replace the lost ones. In contrast, in the non-regenerative form, anemia develops because the bone marrow cannot produce red blood cells (or too few) to replace those that are lost. In cats, the presence of both forms at the same time is possible, which complicates the course of the disease.
Signs of anemia in cats
Pallor. The most common sign of anemia in cats is pale mucous membranes in the mouth and around the eyes. However, this symptom is not necessarily evidence of anemia, since pallor can be caused by other causes.
Weakness. Sick animals exhibit lethargic behavior, as severe anemia can cause weakness.
Rapid heartbeat and breathing. Anemia, especially advanced, leads to an increase in heart rate (tachycardia) and rapid breathing (tachypnea).
Picacism. Anemic cats often exhibit pica (from pica, eating normally inedible substances). Most often, they lick plaster, eat litter from the toilet tray or excrement.
Jaundice. In some cats, anemia manifests itself in the form of jaundice - the mucous membranes become yellowish. Although this symptom usually indicates liver disease, it can also occur with a strong sudden destruction (hemolysis) of red blood cells.
In addition to these signs associated with anemia, the cat may also show signs of an underlying disease (such as chronic kidney disease) that caused the anemia. Cats that develop anemia gradually over time are often able to adapt to it, with little to no symptoms (until the anemia becomes severe enough). In the case of rapid development, the signs appear much more clearly.
Possible causes of anemia in cats.
Anemia due to blood loss:
- Injury;
- Bleeding from ulcers or tumors;
- Bleeding due to poor clotting;
Bleeding can be overt or covert, such as within the body or in the gastrointestinal tract, where it is much more difficult to detect.
Hemolytic anemia:
- Infection with the feline leukemia virus (Feline leukaemia virus, FeLV);
- Feline infectious anemia, hemobartonellosis. Infection caused by Mycoplasma haemofelis (formerly known as Haemobartonella Felis) or other similar organisms;
- Immune hemolytic anemia. In this case, the red blood cells are attacked by their own immune system;
- Toxication. Occurs when eating, for example, onions or onion-containing products, paracetamol (acetaminophen);
- Increased instability of erythrocytes. Occurs, for example, in a disease known as pyruvate kinase deficiency. Most often found among cats of the Abyssinian and Somali breeds;
- Low levels of phosphate in the cat's blood;
- Blood transfusion with an incompatible group;
- neonatal isoerythrolysis. A disease that occurs in newborn kittens, with incompatibility of the blood types of a kitten and a nursing cat;
non-regenerative anemia.
- Infection with the feline leukemia virus (Feline leukaemia virus, FeLV);
- Feline immunodeficiency virus (FIV) infection
- Violation of the bone marrow;
- Erythrocyte aplasia (decrease in the production of red blood cells by the bone marrow);
- Leukemia (white blood cell cancer that can affect the bone marrow);
- Chronic kidney disease;
- iron deficiency;
- Chronic (long-term) inflammatory diseases;
Diagnosis of anemia in cats.
Anemia is confirmed by finding a decrease in the number of red blood cells (and a decrease in hemoglobin concentration) in the cat's blood sample. A decrease in the level can be detected using special devices that directly count red cells. In a simpler way, the fraction of blood volume per red blood cell (hematocrit) is measured. The hematocrit value is obtained by placing a thin glass tube with a blood sample into a centrifuge and determining the volume of red blood cells precipitated at the bottom of the tube.
After anemia is confirmed in a cat, its form is determined - regenerative or not. Features of the regenerative form are:
- A change in the size of red blood cells (called anisocytosis) caused by the presence in the cat's blood of a certain number of large and immature red blood cells released from the bone marrow;
- The presence of reticulocytes (immature red blood cells). With the help of special dyes, these cells can be distinguished from normal (mature) erythrocytes, and by determining their number, it can be assessed whether the anemia is regenerative;
Correct definition of the form of anemia helps to narrow down the list of possible underlying causes that caused anemia. Regenerative anemia is usually caused by either increased breakdown of red blood cells (hemolysis) or blood loss (for example, from excessive bleeding). Non-regenerative anemia usually develops as a consequence of other problems that interfere with the normal production of red blood cells by the bone marrow.
Additional examinations of cats with anemia.
Due to the large number of diseases that can cause various forms of anemia in cats, additional testing is often required to determine the specific cause. These tests may include blood tests to look for agents of infection (such as FeLV, FIV, and Mycoplasma haemofelis), tests to check blood clotting and iron levels, and checks for chronic kidney disease. Some cats require x-rays and ultrasounds, and if bone marrow problems are suspected, bone marrow sampling (aspiration or biopsy) is required. This procedure is carried out for a short general anesthesia, using a needle inserted into the cat's bone.
Treatment of anemia in cats.
Management of anemia in cats consists of symptomatic and supportive care for the cat, as well as specific interventions focused on treating the underlying disease.
Supportive care may include blood transfusions (for severe anemia) and general supportive procedures. As with humans, it is important for cats to know the blood type of the donor and recipient to ensure they are compatible.
Depending on the specific cause of anemia for a cat, healing procedures. Antibiotics are used to treat some infections (such as Mycopalsma haemofelis). With immune destruction of red blood cells - immunosuppressants (for example, corticosteroids). For iron deficiency anemia - preparations for cats containing iron, etc.
The prognosis for treating anemia in cats depends on the cause. The disease in many cases responds well to treatment, but sometimes, especially in severe non-regenerative anemia caused by bone marrow disease, the long-term prognosis can only be very cautious.
Erythrocyte indicators and their significance in the diagnosis of anemia. Regenerative and non-regenerative anemia in animals.
Blood is made up of plasma and shaped elements. Erythrocytes are the most numerous group of blood cells. They are biconcave non-nuclear discs (discocytes) in many mammals. In animals of the camel family, erythrocytes are elliptical in shape (ovalocytes), are not biconcave. Also in birds, reptiles, amphibians, erythrocytes are elliptical, but larger and contain a nucleus.
Erythrocyte indicators (indices) are calculated values that allow us to quantitatively characterize important indicators of the state of erythrocytes. They include the average volume of an erythrocyte (MCV), the average hemoglobin content in an erythrocyte (MCH), the average concentration of hemoglobin in erythrocytes (MCHC), as well as the distribution of erythrocytes in magnitude (RDW), the concentration of hemoglobin in a single erythrocyte.
Hemoglobin
Complex protein - chromoprotein, consisting of protein globin and iron porphyrin - heme. It is a red iron-containing blood pigment, located in erythrocytes, accounting for up to 94% of their dry residue. Hemoglobin performs 2 main functions - gas exchange and regulation of the acid-base state of the body. The hemoglobin content is determined spectrophotometrically using the cyanmethemoglobin method used in most automated systems. It is measured in g / l or in g / dl (g / l * 0.1).
Reasons for an increase in hemoglobin concentration:
1. Myeloproliferative diseases (erythremia);
2. Erythrocytosis;
3. Dehydration;
Reasons for a false increase in hemoglobin concentration:
1. Hypertriglyceridemia;
2. High leukocytosis;
3. Progressive liver diseases;
4. Sickle cell anemia (appearance of hemoglobin S);
5. Multiple myeloma (with multiple myeloma (plasmocytoma) with the appearance of a large number of easily precipitating globulins).
Decrease in concentration- all types of anemia, hyperhydration.
Hematocrit(
HCT, Ht-indicator of the ratio of erythrocyte volume to plasma volume, expressed as a percentage or l / l. The hematocrit is determined using a hematological analyzer in terms of the number of erythrocytes and the average erythrocyte volume (accuracy up to 1%) and the centrifugal method (by centrifugation of blood in hematocrit capillaries, but the results may be overestimated by 1-3% due to the impossibility complete removal plasma between cells). The hematocrit is approximately 3 times lower than the level of hemoglobin (g / l). The fetus is higher than in adults (many large red blood cells).
The standard interval may vary depending on the breed and type of animal. In "hot", energetic horses, the hematocrit is usually higher than in draft horses, since the former have a much larger spleen.
Standard spacing
Higher in greyhounds (49-65%). Slightly elevated hematocrit sometimes occurs in individual specimens of dogs of such breeds as a poodle, German Shepherd, boxer, beagle, dachshund, chihuahua.
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Hematocrit Ht(%) |
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Hematocrit(%) |
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Guinea pig |
Hematocrit depends on the number and volume of red blood cells. And is important in determining blood viscosity. The more red blood cells in the blood, the more friction they create, interacting with the walls of blood vessels and with each other. With an increase in hematocrit, there is a significant increase in blood viscosity . Hematocrit is determined by:
- In the diagnosis of anemia and polycythemia and to evaluate the effectiveness of their treatment.
- To determine the degree of dehydration.
- As one of the criteria for deciding on the need for a blood transfusion.
- To evaluate the effectiveness of blood transfusions.
The hematocrit reflects the ratio of red blood cells to plasma, not the total number of red blood cells. For example, in animals in shock due to blood clotting, hematocrit may be normal or even high, although due to blood loss, the total number of red blood cells may be significantly reduced. Therefore, hematocrit cannot be used to assess the degree of anemia shortly after blood loss or blood transfusion.
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Elevated hematocrit |
Decreased hematocrit |
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- Erythrocytosis 1. primary - myeloproliferative disorder (erythremia) (increases to 55-65%); 3. secondary (increases to 50-55%), hypoxia with a compensatory increase in erythropoietin production: high altitude, chronic lung disease, heart defects with right-to-left blood bypass, chronic methemoglobinemia (rare in dogs and cats); Inadequate production of erythropoietin: tumors and cysts of the kidneys, hydronephrosis, extrarenal tumors that secrete erythropoietin, similar proteins and hormones that can enhance its effects; 3. Relative (false) Dehydration (diarrhea, vomiting, diabetes, toxicosis, excessive diuresis, sweating, drinking restriction, with increased vascular permeability (proteins and water leave tissues (endotoxin shock); Reducing the volume of circulating plasma (a large number of cellular elements, the presence of giant thromboplasts, peritonitis, burn disease); Contraction of the spleen (excitement, fear, pain); With prolonged compression of the vein with a tourniquet during blood sampling. |
-anemia(may decrease to 25-15%) - bleeding, Hemoglobin synthesis disorders (sickle cell anemia, thalassemia), Destruction of erythrocytes as a result of hemolysis - the destruction of erythrocytes inside the body (due to a hereditary defect in erythrocytes, as a result of the appearance of antibodies to one's own erythrocytes or toxic effects), etc .; Increase in circulating plasma volume (cardiovascular and kidney failure, hyperproteinemia); Chronic inflammation, trauma, starvation, oncology, chronic hyperazotemia; Hemodilution (intravenous fluids, especially when kidney function decreases); Second half of pregnancy; Oncological diseases bone marrow or metastases of other tumors in the bone marrow, leading to a decrease in the synthesis of red blood cells, destruction. Hematocrit may decrease slightly when taking blood in the supine position. |
The ability of the spleen to contract and expand can cause significant changes in hematocrit, especially in dogs and horses.
Causes of a 30% increase in hematocrit in cats, 40% in dogs and 50% in horses due to contraction of the spleen:
1. Physical activity immediately before taking blood;
2. Excitement before taking blood.
Reasons for a drop in hematocrit below the standard range due to spleen enlargement:
1. Anesthesia, especially when using barbiturates.
If, in the absence of signs of dehydration, the hematocrit is slightly or moderately elevated, then probable cause erythrocytosis is considered a contraction of the spleen.
If, with the same Hb values, the concentration of proteins in the plasma is increased, then dehydration is likely.
Most full information gives a simultaneous assessment of hematocrit and total protein concentration in plasma.
Normal
ht
1. Loss of protein through the gastrointestinal tract;
2. Priteinuria;
3. Severe liver disease;
4. Vasculitis.
b) The normal concentration of total protein in plasma is the normal state.
1. Increasing protein synthesis;
2. Anemia masked by dehydration.
High
ht
a) Low concentration of total protein in plasma - a combination of "shrinkage" of the spleen with loss of protein.
1. "Reduction" of the spleen;
2. Primary or secondary erythrocytosis;
3. Hypoproteinemia masked by dehydration.
c) High concentration of total protein in plasma - dehydration.
Short
ht
a) Low concentration of total protein in plasma:
1. Significant in this moment or recent blood loss
2. Over-hydration.
b) Normal concentration of total protein in plasma:
1. Increased destruction of red blood cells;
2. Decreased production of red blood cells;
3. Chronic blood loss.
c) High concentration of total protein in plasma:
1. Anemia in inflammatory diseases;
2. Multiple myeloma;
3. Lymphoproliferative diseases.
Average erythrocyte volume
MCV (mean corpuscular volum) - average corpuscular volume - average value the volume of red blood cells, measured in femtoliters (fl) (10 -15 / l) or cubic micrometers.
The most reliable value is given by direct determination using an electronic cell counter. MCV is also determined by the formula as the ratio of hematocrit to the number of red blood cells.
MCV \u003d (Ht (%): number of red blood cells (10 12 / l)) x10
MCV values within the normal range characterize the erythrocyte as a normocyte, less than the normal interval - as a microcyte, more than the normal interval - as a macrocyte.
MCV may vary depending on species, age and physical activity. AND is not reliable with a large number of erythrocytes with a changed shape, abnormal erythrocytes (for example, sickle cells) (MCV may be normal if the patient has both macrocytosis and microcytosis). It should be remembered that microspherocytes have a diameter less than normal, while their average volume often remains normal, so it is always necessary to make a blood smear microscopy.
Macrocytosis (high MCV values) - causes:
1. Hypotonic nature of water and electrolyte balance disorders;
2. Regenerative anemia;
3. Non-regenerative anemia due to impaired immune system and/or myelofibrosis (in some dogs);
4. Myeloproliferative disorders;
5. Regenerative anemia in cats - carriers of the feline leukemia virus;
6. Idiopathic macrocytosis (without anemia or reticulocytosis) in Mini Poodles;
7. Hereditary stomatocytosis (dogs, with a normal or slightly increased number of reticulocytes);
8. Hyperthyroidism in cats (slightly elevated with normal or elevated hematocrit);
9. Newborn animals.
False macrocytosis:
1. Artifact due to erythrocyte agglutination (in immune-mediated disorders);
2. Persistent hypernatremia (when blood is diluted with a liquid before counting the number of red blood cells in an electric meter);
3. Long-term storage of blood samples.
Microcytosis (low MCV values
)
- causes:
1. Hypertonic nature of the violation of water and electrolyte balance;
2. Iron deficiency anemia due to chronic bleeding in adult animals (about a month after their onset due to the depletion of iron in the body);
3. Iron deficiency alimentary anemia in suckling animals;
4. Primary erythrocytosis (dogs);
5. Long-term therapy with recombinant erythropoietin (dogs);
6. Violations of heme synthesis - prolonged deficiency of copper, pyridoxine, lead poisoning, medicinal substances(chloramphenicol);
7. Anemia in inflammatory diseases (MCV is slightly reduced or in the lower normal range);
8. Portosystemic anastomosis (dogs with normal or slightly reduced hematocrit)
9. Portosystemic anastomosis and hepatic lipidosis in cats (mild decrease in MVC);
10. May be with myeloproliferative disorders;
11. Violation of erythropoiesis in English Springer Spaniels (in combination with polymyopathy and heart disease);
12. Persistent elliptocytosis (in crossbred dogs as a result of the absence of one of the proteins in the erythrocyte membrane);
13. Idiopathic microcytosis in some breeds of Japanese Great Danes (Akita and Shiba) - not accompanied by anemia.
False microcytosis - causes (only when determined in an electronic counter):
1. Severe anemia or severe thrombocytosis (if platelets are taken into account with MCV when counting with an electronic counter);
2. Persistent hyponatremia in dogs (due to erythrocyte shrinkage when diluting blood in vitro to count erythrocytes in an electronic counter).
The average concentration of hemoglobin in cells (erythrocytes) (
MCHC -mean cell hemoglobin concentration - an indicator of erythrocyte saturation with hemoglobin, unlike MCH, characterizes not the amount of hemoglobin in the cell, but the “density” of filling the cell with hemoglobin.
In hematology analyzers, the value is calculated automatically or calculated by the formula: MCHC \u003d (Hb (g \ dl) \ Ht (%)) x100(as the ratio of total hemoglobin to hematocrit), expressed in g / dl or in g / l.
Or MCHC= Hb (g\l)*1000\MCV(fl)* RBC(number of erythrocytes)*10 -12 |l
Standard intervals, calculated from the hematocrit value, which is determined using an electronic counter, are slightly higher than with the centrifugation method.
MCHC is the most sensitive indicator for disorders of hemoglobin formation. In addition, it is one of the most stable hematological indicators, so the MCHC is used as an indicator of analyzer errors.
A significant increase in the concentration of hemoglobin in erythrocytes is impossible, since if the cell is too saturated with hemoglobin, it is destroyed. Therefore, overestimated MCHC results indicate errors in the analyzer operation.
Increased MCHC - Causes
In newborns
Spherocytic anemia.
False increase in MCHC (artifact) - causes:
1. Hemolysis of erythrocytes in vivo and in vitro;
2. Lipemia;
3. The presence of Heinz bodies in erythrocytes;
4. Agglutination of erythrocytes in the presence of cold agglutinins (when counting in an electric meter).
Decrease in MCHC - reasons:
1. Regenerative anemia (if there are many stress reticulocytes in the blood);
2. Chronic iron deficiency anemia;
3. Hereditary stomatocytosis (dogs) (due to increased water content in the cell);
4. Hypoosmolar disorders of water and electrolyte metabolism.
When determined using electronic cell counters, the MCHC value in the case of weak microcytosis usually corresponds to normal, but usually decreases if the SEA is significantly below the norm.
False MCHC Downgrade - in dogs and cats with hypernatremia (because the cells swell when blood is diluted before counting in an electronic counter).
The average content of hemoglobin in a cell (erythrocyte)(
MCH- mean cell hemoglobin. It is measured in picograms (10 -12) per erythrocyte and is calculated as the ratio of hemoglobin to the number of erythrocytes. MCH \u003d Hb (g / l) / number of red blood cells (x10 12 / l)It usually correlates directly with the value MCV, except for the presence of macrocytic hypochromic erythrocytes in the blood. MCH corresponds to the color indicator that was used earlier, but more accurately reflects the synthesis of Hb and its level in the erythrocyte. Normally, MCH in the erythrocyte is the basis for differential diagnosis anemia. Based on this index, they can be divided into normo-, hypo- and hyperchromic.
Hypochromia is due to a decrease in the volume of red blood cells (microcytosis) or a decrease in the level of hemoglobin in a red blood cell of normal size. Those. hypochromia can be combined both with a decrease in the volume of erythrocytes, and can be observed with normo- and macrocytosis. Hyperchromia does not depend on the degree of saturation of erythrocytes with hemoglobin, but is due only to the volume of red blood cells, because. an increase in the concentration of hemoglobin above physiological may result in its crystallization and hemolysis of the erythrocyte.
Distribution of erythrocytes by size(RDW
Red cell distribution width
)(width of erythrocyte distribution by volume)
serves as an indicator of the heterogeneity of the size (diameter) or volume of erythrocytes, determined by the electronic method. Depending on the analyzers, there are different variants calculation of this index. RDW-CV (coefficient of variability) is measured in % and shows how much the volume of red blood cells deviates from the average. RDW-SD (standard deviation) is measured in fl and shows the difference between the smallest RBC and the largest.
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REV will increase when the degree of anisocytosis increases, with regenerative anemia (due to reticulocytes and young red blood cells), with iron deficiency anemia (in the phase when red blood cells have a normal and altered size). As with the determination of MCV, the number of large red blood cells in the blood must reach a certain level for the RDW to go beyond the standard range. In some animals, RDW increases earlier than MCV. As the animal's response to anemia develops, immature erythrocytes become predominant, and the RDW value begins to decrease even with the still high MCV value. The reasons for the increase in RDW may be erythrocyte fragmentation occurring in some disorders, when transfused with blood from a donor animal whose MCV differs from that of the recipient; in dogs with hereditary stomatocytosis. Animals with non-regenerative anemia may have a normal RDW value if there are no significant disorders of erythropoiesis . Artificial overestimation of RDW can be in the case of erythrocyte agglutination, in animals with a severe form of anemia, when platelets are included in the calculation of the distribution of cell volume along with erythrocytes.
Histogram of erythrocyte volume and cytograms of erythrocytes. Deviation of MCV and MCV indicators from the norm does not allow identifying the presence of erythrocytes with a changed volume or hemoglobin concentration. Electronic cell counters, in addition to counting their number, are able to determine and graph the volume of individual erythrocytes. Based on the analysis of the histogram, one can judge an increase in the number of microcytes or macrocytes even in cases where the MCV value is within the normal range.
Some devices allow you to determine
concentration of hemoglobin in individual erythrocytes (width of distribution of hemoglobin in an erythrocyte)
By deviation laser beam, passing through individual cells. Studying the histogram of hemoglobin concentrations makes it possible to detect an increase in the number of hypochromic erythrocytes, even if the CKG is normal. An additional characteristic of individual erythrocytes can also be obtained by constructing a cytogram showing the relationship between the volume of individual erythrocytes and the concentration of hemoglobin contained in them.
Classification of anemia by erythrocyte parameters, taking into account the average erythrocyte volume (MCV) and the average concentration of hemoglobin in the cell (MCHC)
Depending on the size of red blood cells, macrocytic, normocytic and microcytic anemia are distinguished. Anemias are classified according to their magnitude as normochromic and hypochromic. Hyperchromic anemia does not exist, because high values of SKGC are an artifact.
a) Anemia normocytic normochromic:
- Acute hemolysis in the first 1-4 days (before the appearance of reticulocytes in the blood);
- Acute bleeding in the first 1-4 days (before the appearance of reticulocytes in the blood in response to anemia);
- Moderate blood loss that does not stimulate a significant bone marrow response;
- Early period iron deficiency (there is still no predominance of microcytes in the blood);
- chronic inflammation(may be mild microcytic anemia);
- Chronic neoplasia (may be mild microcytic anemia);
- Chronic kidney disease (with insufficient production of erythropoietin);
- Endocrine insufficiency (hypofunction of the pituitary gland, adrenal glands, thyroid gland or sex hormones);
- Selective erythroid aplasia (congenital and acquired, including as a complication of vaccination against parvovirus in dogs infected with feline feline leukemia virus, when using chloramphenicol, long-term use of recombinant human erythropoietin);
- Aplasia and hypoplasia of the bone marrow various genesis;
- Lead poisoning (anemia may not be);
- Deficiency of cobalamin (vitamin B12) (develops with a congenital defect in the absorption of the vitamin, severe malabsorption or intestinal dysbacteriosis).
b) Macrocytic normochromic anemia:
- Regenerative anemia (the average concentration of hemoglobin in the erythrocyte is not always reduced);
- For infections caused by feline leukemia virus without reticulocytosis (usually);
- Erythroleukemia (acute myeloid leukemia) and myelodysplastic syndromes;
- Non-regenerative immune-mediated anemia and/or myelofibrosis in dogs;
- Macrocytosis in poodles (healthy mini poodles without anemia);
- Cats with hyperthyroidism (weak macrocytosis without anemia);
- Folate (folic acid) deficiency - rare;
- Congenital disorders of erythropoiesis in Harford calves;
- Pseudoanemia with erythrocyte agglutination (usually also increased SMBK).
c) Macrocytic hypochromic anemia:
- Regenerative anemias with marked reticulocytosis;
- Hereditary stomatocytosis in dogs (often mild reticulocytosis);
- Increased osmotic instability of Abyssinian and Somali erythrocytes (reticulocytosis is usually present);
- False anemia due to prolonged storage of a blood sample;
- False anemia in cats and dogs with persistent hypernatremia.
d) Anemia microcytic or normocytic hypochromic:
- Chronic iron deficiency (months in adult animals, weeks in sucklings);
- Portosystemic shunts in dogs and cats (often without anemia);
- Anemia in inflammatory diseases (usually normocytic);
- Hepatic lipidosis in cats (usually normocytic);
- Normal condition for Japanese dogs Akita and Shiba (without anemia);
- Long-term treatment with recombinant human erythropoietin (moderate anemia);
- Copper deficiency (rare);
- Drugs or agents that inhibit heme synthesis;
- Myeloproliferative disorders with impaired iron metabolism (rarely);
- Pyridoxine deficiency;
- Familial disorder of erythropoiesis in English Springer Spaniels (rare);
- Hereditary elliptocytosis in dogs (rare);
- False anemia when platelets are included in the erythrocyte histogram;
- False anemia in dogs with persistent hyponatremia.
TO Evaluation of erythrocyte indices allows you to get an idea about the characteristics of erythrocytes, which is very important in determining the type of anemia. Erythrocyte indices often respond quickly to anemia treatment and can be used to assess the effectiveness of therapy.
Regenerative and non-regenerative anemia.
The most important approach in the classification of anemia is to find out from the blood picture whether the bone marrow responds to anemia. For this purpose, the absolute reticulocyte count (ARC) is determined (with the exception of horses, their bone marrow is examined).
At healthy dogs and pigs, up to 1.5% of reticulocytes can normally be present, they can also be found in cats. But they are not normally found in horses, cattle, goats.
In cats, reticulocytes are divided into aggregate (large clumps of ribosomes are visible in the cells) and granular (separate small inclusions, apparently the process of maturation of reticulocytes is slower). In cats with moderate anemia, the number of granular reticulocytes may be increased with a normal content of aggregate ones. refers to the aggregate type. It takes about 4 days for the development of reticulocytosis.
Manual RBC counting can be misleading if there is moderate or severe anemia, as reticulocyte count is expressed as a % of total red blood cell count, reticulocyte count must be adjusted for the degree of anemia.
Ht of the given animal/average Ht normal*calculated number of reticulocytes (%).
Corrected reticulocyte count allows you to determine the true increase or not.
A decrease in hematocrit usually leads to an increase in plasma erythropoietin concentration and an increase in absolute blood reticulocyte count (except in horses) if the bone marrow responds to anemia.
In hemolytic anemia, AFR is usually higher than in bleeding (plasma iron concentration is higher).
In severe anemia, basophilic macroreticulocytes (stressed, reticulocytes at an earlier stage of development) may enter the bloodstream. Some of them may mature into macrocytes (in cats).
Absolute Reticulocyte Count (in µl) = RBC Count (in µl)*Reticulocyte Count (%)
It can also be determined using automatic analyzers.
Severe anemia stimulates the production of red blood cells more strongly. In animals with low hematocrit, if the bone marrow responds correctly, the ACR should be increased.
regenerative reaction
Anemia is indicated by the ratio of myeloid and erythroid elements (M / E) below 0.5 and the number of reticulocytes in the bone marrow is more than 5%.
Signs of regenerative anemia
Increased polychromasia (due to an increased number of reticulocytes, with moderate anemia, cats may be absent, because there may be granular reticulocytes);
Increased anisocytosis (but it can also be with some non-regenerative anemia, in horses in the absence of polychromasia with severe regenerative anemia);
The presence of nucleated erythrocytes (rubrycytes and metarubrycytes), but can also be in disorders of an anemic and non-anemic nature with the absence or minimal number of reticulocytes.)
Basophilic granulation in ruminants;
There are species differences in the ability to increase the production of red blood cells (in dogs, the bone marrow response is stronger than in cats and the hematocrit returns to normal faster, then hematocrit in cows, then in horses.)
Anemias that are not accompanied by an increase in the number of reticulocytes or characterize their low content are classified as non-regenerative and weakly regenerative.
To clarify the nature of non-regenerative anemia, it is often necessary to study bone marrow biopsies.
A)
Non-regenerative anemia, not accompanied by leukopenia or thrombocytopenia - in the case of a bone marrow disorder spreading only to erythroid cells.
Causes:
1. Chronic illness kidneys - lack of primary erythropoietin;
2. Endocrine insufficiency (mild anemia):
- hypothyroidism;
- hypoadrenocorticism;
- hypopituitarism;
- hypoandrogenism.
3. Chronic inflammatory diseases (mild to moderate anemia, inflammation, neoplastic processes (tumor));
4. Violation of the synthesis of nucleic acids (hereditary deficiency):
- folate deficiency;
- cobalamin deficiency;
5. Violation of heme synthesis:
- deficiency of iron, copper, pyridoxine;
- lead poisoning;
- medicinal agents.
6. Immune-mediated:
- non-regenerative anemia (development stops at the stage of polychromatophilic erythrocyte or earlier);
- selective erythroid hypoplasia and aplasia (congenital and acquired, including as a complication of vaccination against parvovirus in dogs infected with feline leukemia virus, high doses of chloramphenicol);
- erythroid aplasia with prolonged treatment with recombinant human erythropoietin;
7. Violation of erythropoiesis:
- hereditary disorder in Harford calves and English Springer Spaniels;
- chemotherapeutic agents (vincristine);
- idiopathic disorder in dogs;
- erythroleukemia and myelodysplastic syndromes with a predominance of an erythroid defect (especially in cats), but leukopenia and thrombocytopenia usually occur;
b)
Non-regenerative anemias accompanied by leukopenia and thrombocytopenia (pancytopenia)
Indicate that the bone marrow is either depleted of cells or poorly saturated (hypoplasia (bone marrow is more than 75% fat) and aplasia (absence or marked decrease in hematopoietic cells of all types - erythrocyte, granulocytic and megakaryocytic)), or in it instead of normal hematopoietic precursor cells, a large number of pathologically altered cells (myelophthisis) are present. Pancytopenia is sometimes observed in the terminal stage of cytozoonosis in cats and in septicemia in animals with anemia (utilization or destruction of peripheral blood cells).
Anemia with generalized bone marrow aplasia aplastic. With a decrease in the number or absence of cells of only one line, more specific terms are used to designate a defect - granulocytic hypoplasia, erythroid aplasia, etc.
hypoplasia and aplasia arise as a result of:
- insufficient number of stem cells;
- with violations of the hematopoietic microenvironment;
- disorders of humoral or cellular regulation.
1. Cytotoxic damage to the red bone marrow:
Bracken-fern poisoning (cattle);
- cytotoxic anticancer chemotherapy drugs and radiation;
- administration of exogenous estrogens (dogs and ferrets) and high levels of endogenous estrogen (produced by Sertoli cell tumors, interstitial cells and granulosa cell tumors (dogs), possibly cystic ovaries in dogs, prolonged estrus in ferrets;
- cytotoxic drugs: chloramphenicol (cats usually without anemia), phenylbutazone (dogs and possibly horses), trimetoptim-sulfadiazine (dogs), albendazole (dogs), griseofulvin (cats), trichlorethylene (cattle), may be - thiacetarsemide, meclofenamic acid and quinidine (dogs);
2. Infectious agents:
- Ehrlichia spp. (dogs, horses, cats);
- parvovirus (dog puppies);
- infection with feline leukemia virus;
- panleukopenia (cats);
3. Congenital - in calves and foals (treatment of pregnant females with sulfonamides, pyrimethamine), hereditary - in foals.
4. Immune-mediated - idiopathic aplastic anemia (dogs, cats, horses).
Myelophthisis(a disorder characterized by the replacement of hematopoietic cells with abnormal cells and changes in the microenvironment in the bone marrow):
- myelogenous and lymphoid leukemias;
- multiple myeloma;
- myelodysplastic syndromes (increased apoptosis);
- myelofibrosis (often associated with anemia and rarely with pancythemia);
- osteosclerosis;
- metastatic lymphomas;
- metastatic mast cell tumors.
Anemia- this is a pathological condition of the body, which is characterized by a decrease in the number of red blood cells and hemoglobin in a unit of blood. Erythrocytes are formed in the red bone marrow from protein fractions and non-protein components under the influence of erythropoietin (synthesized by the kidneys). Erythrocytes for three days provide transport, mainly oxygen and carbon dioxide, as well as nutrients and metabolic products from cells and tissues. The life span of an erythrocyte is one hundred and twenty days, after which it is destroyed. Old erythrocytes accumulate in the spleen, where non-protein fractions are utilized, and protein enters the red bone marrow, participating in the synthesis of new erythrocytes.
The entire cavity of the erythrocyte is filled with protein, hemoglobin, which includes iron. Hemoglobin gives red blood cells their red color and also helps them carry oxygen and carbon dioxide. Its work begins in the lungs, where red blood cells enter with the bloodstream. Hemoglobin molecules capture oxygen, after which oxygen-enriched erythrocytes 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; by reducing the number of red blood cells, the transport of oxygen and carbon dioxide is disrupted. As a result, a person may experience signs of anemia such as 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. That is why anemia is an important symptom that requires the necessary research to identify the underlying cause that led to its development.
Severe forms of anemia due to tissue hypoxia can lead to serious complications such as shock conditions (eg, hemorrhagic shock), hypotension, coronary or pulmonary insufficiency.
Anemia classification
Anemias are classified:
- according to the mechanism of development;
- by severity;
- by color indicator;
- on a morphological basis;
- on the ability of the bone marrow to regenerate.
Classification | Description | Kinds |
According to the mechanism of development | According to the pathogenesis, anemia can develop due to blood loss, impaired formation of red blood cells, or due to their pronounced destruction. | According to the mechanism of development, there are:
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By severity | Depending on the level of decrease in hemoglobin, there are three degrees of severity of anemia. Normally, the hemoglobin level in men is 130 - 160 g / l, and in women 120 - 140 g / l. | There are following degrees of severity of anemia:
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By color index | The color indicator 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 index:
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According to morphological features | With anemia, red blood cells of various sizes can be observed during a blood test. Normally, the diameter of erythrocytes should be from 7.2 to 8.0 microns ( micrometer). Smaller RBCs ( microcytosis) can be observed in iron deficiency anemia. Normal size may be present when posthemorrhagic anemia. Larger size (macrocytosis), in turn, may indicate anemia associated with a deficiency of vitamin B12 or folic acid. | Classification of anemia by morphological features:
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According to the ability of the 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 ( erythrocyte precursors) in blood. Also, their level indicates how actively the formation of red blood cells proceeds ( erythropoiesis). Normally, in human blood, the number of reticulocytes should not exceed 1.2% of all red blood cells. | According to the ability of the bone marrow to regenerate, the following forms are distinguished:
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Causes of anemia
There are three main causes leading to the development of anemia:
- blood loss (acute or chronic bleeding);
- increased destruction of red blood cells (hemolysis);
- reduced production of red blood cells.
Factors affecting 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 medicines |
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Iron-deficiency anemia
Iron deficiency anemia is hypochromic anemia, which is characterized by a decrease in the level of iron in the body. Iron deficiency anemia is characterized by a decrease in red blood cells, hemoglobin and a color index.
Iron is vital important element involved in many metabolic processes in the body. In a person weighing seventy kilograms, the iron reserve in the body is 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 incoming iron in 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 |
Violation of the intake of iron in the body |
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Impaired absorption of iron | Iron absorption occurs at the level of the gastric mucosa, therefore, stomach diseases such as gastritis, peptic ulcer or gastric resection lead to impaired iron absorption. |
Increased body's 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 a patient:- anemic syndrome;
- sideropenic syndrome.
- severe general weakness;
- increased fatigue;
- attention deficit;
- malaise;
- drowsiness;
- black stool (with gastrointestinal bleeding);
- heartbeat;
- taste perversion (for example, patients eat chalk, raw meat);
- perversion of smell (for example, patients sniff acetone, gasoline, paints);
- brittle, dull, split ends;
- white spots appear on the nails;
- the skin is pale, the skin is flaky;
- cheilitis (bites) 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 erythrocytes);
- hypochromia of erythrocytes (weak color of erythrocytes);
- poikilocytosis (erythrocytes of various forms).
- decrease in the level of ferritin;
- serum iron is reduced;
- serum iron-binding capacity is increased.
To identify the cause that led to the development of anemia, the following instrumental studies can be prescribed to the patient:
- 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 examine 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 plant products.
Food | Product Names | |
Food |
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While dieting, you should also increase your intake of foods containing vitamin C, as well as meat protein (they increase the absorption of iron in the body) and reduce the intake of eggs, salt, caffeine and calcium (they reduce the absorption of iron).
Medical treatment
In the treatment of iron deficiency anemia, the patient is prescribed iron supplements in parallel with the diet. These drugs are designed to compensate for 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;
- the severity of the disease;
- causes of iron deficiency anemia;
- based on the results of the analyses.
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 for the purpose of accelerated saturation of the body with iron;
- if the patient has intolerance to iron preparations when they are taken orally.
Surgery is performed if the patient has acute or chronic bleeding. So, for example, with 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). With uterine bleeding, as well as with bleeding in organs located in abdominal cavity, laparoscopy may be used.
If necessary, the patient may be assigned a transfusion of red blood cells to replenish the volume of circulating blood.
B12 - deficiency anemia
This anemia is due to a lack of vitamin B12 (and possibly folic acid). Characterized by megaloblastic type ( increased amount megaloblasts, erythrocyte precursor cells) of hematopoiesis and is 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 (Castle's intrinsic factor). This protein protects the vitamin that has entered the body from the negative effects of the intestinal microflora, and also promotes its absorption.
The complex of gastromucoprotein and vitamin B12 reaches the distal (lower) small intestine, where this complex breaks down, absorption of vitamin B12 into the intestinal mucosa and its further entry into the blood.
From the bloodstream, this vitamin comes:
- in the red bone marrow to participate in the synthesis of red blood cells;
- in the liver, where it is deposited;
- to the central nervous system for the synthesis of the myelin sheath (covers the axons of neurons).
Causes of B12 deficiency anemia
Exist the following reasons development of B12 deficiency anemia:- insufficient intake of vitamin B12 with food;
- violation of the synthesis of internal factor Castle due to, for example, atrophic gastritis, gastric resection, gastric cancer;
- intestinal damage, for example, dysbiosis, helminthiasis, intestinal infections;
- increased body needs for vitamin B12 ( fast growth, active sports, multiple pregnancy);
- violation of vitamin deposition due to cirrhosis of the liver.
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.
Name of the syndrome | Symptoms |
Anemia 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:- decrease in the level of red blood cells and hemoglobin;
- hyperchromia (pronounced color of erythrocytes);
- macrocytosis (increased size of red blood cells);
- poikilocytosis ( various shape erythrocytes);
- microscopy of erythrocytes reveals Kebot rings and Jolly bodies;
- reticulocytes are reduced or normal;
- a decrease in the level of white blood cells (leukopenia);
- increased levels of lymphocytes (lymphocytosis);
- decreased platelet count (thrombocytopenia).
A puncture of the red bone marrow revealed an increase in megaloblasts.
The patient may be assigned the following instrumental studies:
- study of the stomach (fibrogastroduodenoscopy, biopsy);
- examination of the intestine (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 for vitamin B12 is three micrograms.
Medical 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 depot of vitamin B12 in the body.
- Subsequently, the patient receives for life intramuscular injections once a week, 500 mcg.
A patient with B12-deficiency anemia should be observed 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, which is partly produced by intestinal cells, but mainly must come from outside to replenish the body's needs. The daily intake of folic acid is 200-400 micrograms.
In foods, as well as in the cells of the body, 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 organism in the prenatal period (contributes to 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 the processes of hematopoiesis;
- together with vitamin B12 is involved in DNA synthesis;
- prevents the formation of blood clots in the body;
- improves the processes of regeneration of organs and tissues;
- participates in the renewal of tissues (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);
- malabsorption of folic acid in 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 has an anemic syndrome (symptoms such as fatigue, palpitations, pallor skin, decreased performance). Neurological syndrome, as well as atrophic changes in the mucous membrane of the oral cavity, stomach and intestines, are absent in this type of anemia.Also, the patient may experience an increase in the size of the spleen.
Diagnosis of folate deficiency anemia
In a general blood test, the following changes are observed:- hyperchromia;
- decrease in the level of red blood cells and hemoglobin;
- macrocytosis;
- leukopenia;
- thrombocytopenia.
Myelogram reveals increased content megaloblasts and hypersegmented neutrophils.
Treatment of folate deficiency anemia
Nutrition in folate deficiency anemia plays a big role, the patient needs to consume foods rich in folic acid daily.It should be noted that with any culinary processing of products, folates are destroyed by approximately fifty percent or more. Therefore, in order to provide the body with the necessary daily rate products are recommended to be consumed fresh (vegetables and fruits).
| Food | Name of products | The amount of iron per hundred milligrams |
| Food of animal origin |
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| Foods of plant origin |
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Drug treatment of folic acid deficiency anemia involves taking folic acid in an amount of five to fifteen milligrams per day. Required dosage is established by the attending physician depending on the age of the patient, the severity of the course of anemia and the results of the studies.
The prophylactic dose includes taking one to five milligrams of the vitamin per day.
aplastic anemia
Aplastic anemia is characterized by bone marrow hypoplasia and pancytopenia (decrease in the number 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 micro-environment. 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 stimulating hematopoiesis;
- not using the hematopoietic tissue of elements important for the body, such as iron and vitamin B12.
- hereditary factor (for example, Fanconi anemia, Diamond-Blackfan anemia);
- drugs (eg, non-steroidal anti-inflammatory drugs, antibiotics, cytostatics);
- chemicals (eg inorganic arsenic, benzene);
- viral infections (eg, parvovirus infection, human immunodeficiency virus (HIV));
- autoimmune diseases (eg, systemic lupus erythematosus);
- severe nutritional deficiencies (eg, vitamin B12, folic acid).
Symptoms of aplastic anemia
The clinical manifestations of aplastic anemia depend on the severity of pancytopenia.With aplastic anemia, the patient has the following symptoms:
- pallor of the skin and mucous membranes;
- headache;
- dyspnea;
- increased fatigue;
- gingival bleeding (due to a decrease in the level of platelets in the blood);
- petechial rash (red spots on the skin of small sizes), 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
In the general blood test, the following changes are observed:- decrease in the number of red blood cells;
- decrease in hemoglobin level;
- decrease in the number of leukocytes and platelets;
- decrease in reticulocytes.
In a biochemical blood test, the following is observed:
- increase in serum iron;
- saturation of transferrin (iron-carrying protein) with iron by 100%;
- increased bilirubin;
- increased lactate dehydrogenase.
- underdevelopment of all germs (erythrocyte, granulocytic, lymphocytic, monocytic and macrophage);
- replacement of bone marrow with fat (yellow marrow).
- ultrasound examination of parenchymal organs;
- electrocardiography (ECG) and echocardiography;
- fibrogastroduodenoscopy;
- colonoscopy;
- CT scan.
Treatment of aplastic anemia
With the right supportive treatment, the condition of patients with aplastic anemia improves significantly.In the treatment of aplastic anemia, the patient is prescribed:
- immunosuppressive drugs (for example, cyclosporine, methotrexate);
- glucocorticosteroids (for example, methylprednisolone);
- antilymphocyte and antiplatelet immunoglobulins;
- antimetabolites (eg, 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;
- no effect of treatment.
Treatment effectiveness | Indicators |
Complete remission |
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Partial remission |
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Clinical Improvement |
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No therapeutic effect |
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Hemolytic anemia
Hemolysis is the premature destruction of red blood cells. Hemolytic anemia develops when the activity of the bone marrow is not able to compensate for the loss of red blood cells. The severity of anemia depends on whether hemolysis of red blood cells began gradually or abruptly. Gradual hemolysis may be asymptomatic, while anemia in severe hemolysis may be life-threatening for the patient and cause angina pectoris, as well as cardiopulmonary decompensation. Hemolytic anemia can develop due to hereditary or acquired diseases.
By localization, hemolysis can be:
- intracellular (for example, autoimmune hemolytic anemia);
- intravascular (eg, 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 erythrocytes;
- defects in the structure and synthesis of hemoglobin protein;
- enzymatic defects in the erythrocyte;
- hypersplenomegaly (enlargement of the liver and spleen).
There are the following hereditary hemolytic anemias:
- enzymopathies (anemia, in which there is a lack of enzyme, deficiency of glucose-6-phosphate dehydrogenase);
- hereditary spherocytosis or Minkowski-Choffard disease (erythrocytes of an irregular spherical shape);
- thalassemia (violation of the synthesis of polypeptide chains that are part of the structure of normal hemoglobin);
- sickle cell anemia (a change in the structure of hemoglobin leads to the fact that red blood cells take on a sickle shape).
Immune disorders are characterized by autoimmune hemolytic anemia.
Non-immune disorders can be caused by:
- pesticides (for example, pesticides, benzene);
- medicines (for example, antivirals, antibiotics);
- physical damage;
- infections (eg malaria).
- defective artificial heart valve;
- disseminated intravascular coagulation;
- hemolytic uremic syndrome;
Symptoms of hemolytic anemia
Symptoms and manifestations of hemolytic anemia are diverse 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.
Symptoms of hemolytic anemia include:
- pallor of the skin and mucous membranes;
- fragility of nails;
- tachycardia;
- increased respiratory movements;
- lowering blood pressure;
- yellowness of the skin (due to an increase in the level of bilirubin);
- ulcers may appear on the legs;
- skin hyperpigmentation;
- gastrointestinal manifestations (eg, abdominal pain, stool disturbance, nausea).
Prolonged hemolysis can lead to the development of gallstones due to impaired bilirubin metabolism. At the same time, patients may complain of abdominal pain and bronze skin color.
Diagnosis of hemolytic anemia
In the general analysis of blood is observed:- decrease in hemoglobin level;
- decrease in the level of red blood cells;
- an increase in reticulocytes.
In a biochemical blood test, there is an increase in the level of bilirubin, as well as hemoglobinemia (an increase in free hemoglobin in the blood plasma).
In children whose mothers suffered from anemia during pregnancy, iron deficiency is also often found by the first year of life.
Symptoms of anemia often include:
- feeling tired;
- sleep disorder;
- dizziness;
- nausea;
- dyspnea;
- weakness;
- fragility of nails and hair, as well as hair loss;
- pallor and dryness of the skin;
- perversion of taste (for example, the desire to eat chalk, raw meat) and smell (the desire to sniff liquids with pungent odors).
At the same time, it should be noted that mild form anemia may not manifest itself in any way, so it is very important to take regular blood tests to determine the level of red blood cells, hemoglobin and ferritin in the blood.
During pregnancy, the norm of hemoglobin is considered to be 110 g / l and above. A drop below normal is considered a sign of anemia.
Diet plays an important role in the treatment of anemia. From vegetables and fruits, iron is absorbed much worse than from meat products. Therefore, the diet of a pregnant woman should be rich in meat (for example, beef, liver, rabbit meat) and fish.
The daily iron requirement 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 | Mode of application |
|
Sorbifer | Ferrous sulfate and ascorbic acid. | As a preventive measure for the development of anemia, it is necessary to take one tablet per day. WITH therapeutic purpose two tablets should be taken daily in the morning and evening. |
Maltofer | iron hydroxide. | In the treatment of iron deficiency anemia, two to three tablets should be taken ( 200 - 300 mg) per day. WITH preventive purpose the drug is taken in one tablet ( 100 mg) in a day. |
Ferretab | Ferrous fumarate and folic acid. | It is necessary to take one tablet per day, if indicated, the dose can be increased to two to three tablets per day. |
Tardyferon | Iron sulfate. | For prophylactic purposes, take the drug, starting from the fourth month of pregnancy, one tablet daily or every other day. For therapeutic purposes, it is necessary to take two tablets a day in the morning and evening. |
In addition to iron, these preparations may additionally contain ascorbic or folic acid, as well as cysteine, as they contribute to better assimilation iron in the body. Before use, you should consult with a specialist.
ANEMIA
Anemia is a condition characterized by inadequate circulation of hemoglobin (Hgb). This is the result of excessive destruction of red blood cells (RBCs), reduction of red blood cells or reduction in their production. Anemia is a manifestation of the underlying disease process. The classification of anemias can be useful for compiling a list of the various diagnoses in a given animal. Anemia can be regenerative or non-regenerative (Table 1).
Regenerative anemia is the red bone marrow's response to an increase in circulating RBCs (erythrocytes). This response is a measure of the number of reticulocytes, immature red blood cells involved in circulation.
Regenerative anemia peculiar a large number of reticulocytes, as well as a decrease in the number of red blood cells and their destruction.
At non-regenerative anemia red bone marrow gives a poor response and the number of reticulocytes is insignificant.
Anemia can be acute and chronic . More often in acute anemia, a decrease in the number of red blood cells or their destruction is characteristic. Chronic anemias are characterized by insufficient production of red blood cells, although slow blood loss (bleeding) can also be the cause. The RBC index is used in the further characterization and classification of anemia.
The value of corpuscular volume (mean volume of erythrocytes - MCV) is an indication of the size of erythrocytes. Mean Cell Volume - MCV (femtoliter) = (PCV- or hematocrit x 10) : RBC (million).
The volume of mature erythrocyte precursors in the red bone marrow decreases as the amount of hemoglobin (Hgb) increases. Therefore, reticulocytes have a higher mean cell volume (MCV) and MCV increases with regenerative anemia. Anemia with a high MCV is classified as macrocytic. A low MCV in anemic adult animals indicates iron deficiency from slow blood loss (usually GJ - gastrointestinal or renal). Low MCV is seen in the Akita and Shiba Inu, which normally have low red blood cell counts. A low volume of erythrocytes is observed in congenital renal abnormalities. The value of the concentration of corpuscular hemoglobin (MCHC) indicates the concentration of hemoglobin in the total volume of erythrocytes. MCHC (g/dl) = (Hgb x 100) : PCV. This gives similar information in terms of the value of corpuscular hemoglobin (MCH), but is considered more accurate. MCH or mean hemoglobin per erythrocyte (picograms) = (Hgb x 10) : RBC (millions). Low hemoglobin concentration (MCHC) along with macrocytosis characterizes regenerative anemia. An insignificant content of MCHC is observed in iron deficiency. Rising MCHC indicates hemolysis and laboratory error.
Laboratory diagnosis of anemia is based on concentration or total cell volume (RCV). The next essential test is the reticulocyte count. Reticulocytes are polychromic cells when stained by Wright or Giemsa. Specific staining of reticulocytes - methylene blue staining of living cells. Reticulocytes can be detected within 72 hours after significant blood loss or hemolysis. The peak reticulocyte response is within 5-7 days. Hemolysis (in the red bone marrow) of reticulocytes is usually more affected than hemorrhages due to the drop in iron resulting from RBC destruction. The reticulocyte count is an indication of the degree of regeneration and must be interpreted in relation to PCV. The index of reticulocytes is a rough determination, depending on how the reticulocyte response corresponds to the degree of anemia.
Reticulocyte index = animal PCV x % reticulocytes: normal PCV.
A volume greater than 1 indicates an appropriate response. Cats have a lower rate of reticulocytosis for a specific stage of anemia compared to dogs. Cats produce both punctate and reticulocyte aggregate. The reticulocyte aggregate is polychromatic cells when they are stained according to Wright and one count is made when determining the reticulocyte count.
Evaluation of the red bone marrow RBC response is most accurate with live methylene blue staining and reticulocyte count as a percentage of total RBC. Their absolute number must be determined to prove a response that does not depend on the degree of anemia. For example, 1 ml of blood in a dog normally contains 6.5 x 10 6 RBC with 1% (65,000) reticulocytes; an anemic dog has 2 x 10 6 RBCs with 3% (60,000) reticulocytes. Due to the fact that the production of reticulocytes in dogs in both cases is approximately the same, the response of the dog with anemia is weaker. A good response is > 3 x 10 6 reticulocytes/ml of blood, eg 3 x 10 RBC with 10% reticulocytes.
A simpler method for evaluating erythrocyte response is based on polychromic RBC counts after simple staining or Wright staining. The value of the number of polychrome RBCs is determined for 10 emission fields along the length of separately lying blood smears.
A normal hemogram or unresponsive anemia is 0-1 polychromic RBCs per visual field in a dog; in anemia with an average response of 5 RBC per field of view; with moderate anemia with a response - 5-10 in the field of view; with anemia with a high response of 10-20 per field of view. Much lower numbers (about half of the RBCs in dogs) are seen in cats; in horses, polychromasia (reticulocytosis) is not observed.
In cells/ml can be roughly calculated with a multiple of the number of cells responding to 1 emission field of 8.000, although if you take the value of 10 polychrome RBCs per field, you get 80.000 per 1 ml in the blood. Platelets can be counted in the same way. This method is used when comparing platelets with the number of reticulocytes. See table 6, p. 290 showing the RBC volume level for some types of pets.
PCV and total protein are simultaneously determined due to a decrease in both indicators in cases of anemia with blood loss. Normally, total protein and a decrease in PCV are seen when hemolysis and anemia cause a lack of RBC production.
Medical history and physical examinations are especially important for open causes of anemia. The data of the medical history are different depending on the chronic or acute form of anemia. Acute anemias include sudden attacks of weakness, lethargy, chronic collapse, pallor of the mucous membranes, discoloration of urine, tachypnea and dyspnea. This is usually caused by hemolysis or lack of RBC. Signs of chronic anemia are often vague and include lethargy, depression, and anorexia. Sometimes you can notice the pallor of the mucous membranes, weakness and dyspnea. In many cases, these signs may appear suddenly. Chronic anemias, characterized by slow onset of symptoms and usually non-regenerative, are associated with an increase in RBC production. In all cases, the owner must be asked about possible poisoning by pills or toxin, as well as traumatic incidents.
Medical history and physical examinations, RBC count, total protein, and reticulocyte count should indicate anemia associated with blood loss (regenerative), increased RBC destruction (regenerative), or reduced RBC production (non-regenerative).
Other relevant diagnostic tests are presented in Tables 2,3 and 4.
Signs of a red bone marrow biopsy include non-regenerative anemia, more than one infected cell line, selective neutropenia, selective thrombocytopenia, monoclonal gammopathy, and fever of unknown type.
NON-REGENERATIVE ANEMIA
Nutritional anemia.
In adult animals, this is associated with slow blood GJ lesions such as ulcerative neoplasms, primary ulcers, or intestinal inflammation. Chronic blood loss eventually leads to iron deficiency. Initially there is an attempt at regeneration and later there is a lack of reticulocyte production and the anemia becomes microcytic (low MCV) and hypochromic (low MCHC). Treatment includes blood transfusions (if needed), iron supplements, and addressing the underlying cause.
All animals during the feeding period are deficient in iron, however, this is especially true for pigs. Pigs should be given parenteral iron or RO during the first week of life. These activities should be carried out to rule out vitamin E deficiency; any manifestation of this deficiency in the herd or a previous presence of iron toxicosis (p. 2071) is reason to withhold iron supplementation until 24 hours after taking vitamin E.
Persistent anemia in young pigs that is not related to previous iron supplementation should call for precautions.
Vitamin E is needed for heme synthesis and there is normally a large amount of heme that releases and clears iron from PO or parenteral administration. Low levels of vitamin E, and hence heme, allow free iron to circulate, which results in cell membrane peroxidation and necrosis, particularly in the heart, liver, and skeletal muscle (see Lamb and calf nutritional myopathy, P870, porcine dietary hepatosis, p .872).
Copper deficiency can be absolute or associated with an excessive presence of molybdenum. Copper is needed for the feroxidase enzyme system; deficiency blocks the use of iron, which provokes iron deficiency anemia, which can be hypochromic and microcytic. In anemia with copper deficiency, red bone marrow hemosiderin is normal or exceeds it, but the serum iron content is low. Cobalt and copper are commonly added to feed as supplements and when there is a lack of salt.
Deficiency of vitamin B 6 or pyridoxine reduces heme synthesis and causes anemia, but is not clinically detected and is considered rare.
RED BONE MARROW INSUFFICIENCY
Red bone marrow failure is a plastic anemia characterized by thrombocytopenia, granulocytopenia, and anemia. Because RBCs live slightly longer (100-120 days in dogs, 66-78 days in cats) than neutrophils (8 hours) and platelets (8-10 days), animals with acute plastic anemia show signs of thrombocytopenia (blood loss) or leukopenia (infection). Animals with chronic plastic anemia show signs of anemia.
Hyperred cell aplasia is usually described when only RBCs and their progenitors are affected. Anemia is always a serious condition, and serum iron concentrations are either normal or reduced. Hyperred cell aplasia is usually idiopathic or may be associated with infectious feline leukemia virus or medication (eg, thiacetarsamide soda).
There is evidence that immune reactivity against RBC precursors may lead to this condition.
Treatment of aplastic anemia and hyperred cell aplasia is dictated by hidden causes while supportive measures are taken in the hope of remission. A complete picture is needed, including questions related to exposure to drugs or toxins. Blood transfusions are needed when clinical signs indicate a need for increased oxygen delivery to the tissues. If no specific cause is found, then immunosuppressive levels of corticosteroids are given. Other immunosuppressive drugs may cause remission in some cases of hyperred cell aplasia. Erythropoietin and granulocyte colony-stimulating factor may be useful if RBC and WBC precursors, respectively, are found in red bone marrow examination. The infection is treated with appropriate bactericidal antibiotics. For prophylaxis, antibiotics are prescribed for animals with a neutrophil count less than 1,000/ml.
Anemia in chronic diseases.
Anemia is normocytic, normochromic, and non-regenerative. It is associated with hypothyroidism, decreased adrenocorticoids, kidney disease, liver disease and chronic inflammation or infection, and neoplasia. It can develop 2 weeks after the onset of the disease. Anemia usually subsides (PCV 18-35) and serum iron concentrations fall. A biopsy of the red bone marrow is accompanied by a large amount of iron in the RES cells. Anemia may be due to a combination of several factors, including iron sequestration in RES, reduced production of erythropoietins, and shortened RBC life cycle. Treatment is dictated by the hidden processes of the disease. In the case of renal insufficiency, when there is a definitive deficiency in the production of erythropoietins, an injection of erythropoietin can be very beneficial.
REGENERATIVE ANEMIA
Blood loss .
Blood loss can be subacute, acute, and chronic, and clinical signs depend on the rate of blood volume depletion. Chronic blood loss may be the result of iron deficiency and the development of non-regenerative anemia. In subacute and acute hemorrhages, PCV and total protein are normal. 6 hours is needed to increase tissue circulating volume, after which PCV and total protein decrease. Blood loss can also be external and internal. Internal usually leads to a disproportionate drop in PCV because proteins are reabsorbed into the blood of the vascular system, since the minimum amount of intact RBC has already been reabsorbed. The essence of reticulocytosis is the absence of its occurrence up to 72 hours from the onset of blood loss.
Neoplasms with bleeding into a body cavity or tissue or external bleeding can cause anemia with blood loss that is often subacute in nature. Intermittent weakness and anemia can mean perforating tumors and resulting little blood loss. In these cases, reticulocytosis is present because regeneration time has passed. Hematomas can appear in the same way as ruptured neoplasms.
The initial treatment consists of expanding the volume and moving the RBC when the hemorrhage has already appeared. Prolonged bleeding must be stopped and the latent conditions of the disease eliminated.
Excessive destruction of RBC
Hemolytic anemia can be extra and intravascular. Extravascular hemolysis occurs when RES phagocytizes RBCs. Hemoglobin is converted to bilirubin, resulting in icterus or bilirubinuria. In intravascular hemolysis, RBCs release Hgb into the blood of the vascular system, resulting in hemoglobinemia, hemoglobinuria, and later icterus. Direct and indirect determination of belirubin is not particularly important in hemolytic diseases, except in particularly early stages. Indirect bilirubin is not yet connected by the liver and increases early. Then the liver combines bilirubin and the level of direct bilirubin rises. Because the liver can combine large amounts of bilirubin, normally high indirect bilirubin in the presence of hemolytic diseases and anemia also indicates severe hemolysis or concurrent liver disease.
Extracorporeal anomalies.
Immune hemolytic anemia (JHA): JHA is an increased destruction of the RBC, masked by antibodies or anti-Ab complexes attached to the surface of the RBC. It is characterized by regenerative anemia, spherocytosis (in dogs), and often by the presence of autoantibodies against RBC (positive Coombs test). Primary (indiopathic) JHA involves only the RBCs themselves and occurs in 60-70% of cases in dogs. The high serum concentration of antibodies to viral AH in dogs with primary JHA suggests that idiopathic disease may follow viral infections. One of the implications is the clinical nature of the JHA-associated vaccine temporal relationship in dogs. Secondary JHA is associated with a wide variety of latent conditions. They include immune thrombocytopenia, systemic lupus erythematosus, viral diseases, severe bacterial infections, granulomatosis, lymphosarcoma, lymphocytic leukemia, medication. Medications associated with JHA include trimethoprim sulfa and ornetoprim sulfa in dogs, and methimase and propylthiaurocil in cats.
Clinical signs differ according to the type of hemolysis and the onset of the disease. In the case of simple intravascular hemolysis, the animal may be subject to subacute or acute anemia, hemoglobinemia, hemoglobinuria, sudden weakness, collapse, and shock. Animals with acute or chronic illnesses, including extravascular hemolysis, may be prone to weakness, anemia, and possibly jaundice. Enlargement of the spleen is seen in many animals, as the spleen is usually involved in RBC destruction in the first place.
Laboratory studies also vary on the severity and type of RBC lesions. In subacute cases, there is a lack of reticulocytes. Later, marked reticulocytosis is observed. Primary stimulation of the red bone marrow leads to neutral leukocytosis, to a significant shift to the left. Serum bilirubin levels vary, as do the presence of hemoglobinuria and bilirubinuria. In some cases, RBCs autoagglutinate when blood is in a tube containing an anticoagulant. This can be confirmed microscopically to distinguish it from pharmacy rouleaux, which is not a sign of immune destruction of RBC.
Therapy in JHA is dictated by the increasing destruction of RBC RES and the increase in the production of degrading antibodies. In the case of secondary JHA, the underlying causes must be identified and treated. Immunosuppressive doses of corticosteroids (prednisone 2.2 mg/kg or dexamethasone 0.3 mg/kg) are prescribed to rapidly restore RES. These drugs are maintained at this level until the PCV rises to 30 and then slowly decreases over 2-3 periods. If corticosteroids are not effective, other immunosuppressive drugs such as cyclophosoranide, azatilprine are used. As an adjunct to restoring RES, these drugs increase antibody production faster than corticosteroids. These remedies are indicated in cases of complex autoagglutinations, intravascular hemolysis, complex anemias - they are better than blood transfusions when a blood transfusion is prescribed and when the complex iderus subsides. Other immunosuppressive drugs are permitted, although no controlled studies have been conducted to demonstrate their effectiveness. Recently, human immunoglobulin (0.5 - 1.50/kg, 1V, ca. 12 h period) has been shown to be effective in dogs. Blood transfusions are used when there are clinical grounds for doing so. The use of transfusion (P18) is not associated with an increase in mortality. If a transfusion is performed, mixing of blood types may occur and the animal should be carefully examined. Splenectomy is considered ineffective for JHA in dogs. Plasmapheresis may be particularly effective before cytotoxic therapy produces a favorable response, but this is only possible at specific referral centers.
Isoimmune hemolytic diseases.
This happens when the blood type of the embryo does not match the mother's. Newborn animals receive antibodies due to colostral immunity.
Hemolytic diseases of newborn puppies and kittens.
Spontaneous sensitivity of females and uterus to fetal RBC antigens, which separates the AH of the main blood groups by their incompatibility, is rare. 40% of dogs contain DEA 1 antigen, 90% of cats contain A-AG. Therefore, the chance of mating an animal containing this AG with an animal not containing it is 40/60 in dogs and 90/10 in cats. Diagnosis of maintenance and treatment of kittens and puppies susceptible to hemolytic diseases is related to the principles that will be described below for adult animals.
Hemolytic diseases of newborn calves:
Spontaneous sensitivity of cattle to the fetal RBC antigen is very rare or does not occur at all. Blood vaccines are designed to prevent babiziosis and apaplasmosis and may contain RBC antigens that immunize females. If the bull has the same RBC antigen as the vaccine donor, then the calves can accept these antigens and develop isoimmune hemolytic anemia when receiving colostrum. The pregnancy is proceeding normally. Abs isolated from RBC affected calves are considered JG or in some cases hemolytic. A simple 2ml dose of Babesia vaccine for several weeks prior to calving may result in isoerythrolysis in the neonatal period. And the most fatal cases occur when the female is vaccinated 4-5 times during the year. The Coombs test is usually very positive. Owners may notice red urine in newborn calves and exacerbate the disease problem of re-vaccinating females for suspected neonatal infection.
The disease may be mild or subacute, with symptoms appearing 12 to 48 hours after birth. In subacute cases, death can occur 2 hours after the onset of signs of severe dyspnea and 12 to 16 hours after birth.
Acute cases are characterized by depression, dyspnea, and sometimes fever that develops 24 to 48 hours after birth.
Calves continue to suckle, but weaken, pallor appears, which is hidden for 1-2 days with moderate jaundice.
Death can occur within 4-5 days. Moderately affected calves show reduced activity and lethargy.
In subacute cases, there is hemoglobinuria, hypofibrinogenemia, and large fibrin degradation products, rapid death, spongy spleen, and kidney discoloration. There is an excess of pleural fluid, stained with blood, the lungs are edematous and overflowing with blood. At acute form PCV drops to 6-7% and hemoglobinuria is often observed. Red bone marrow gives an insufficient response; there are 1-2% polychromatophilic RBCs and up to 140 rubricites per 100 WBCs. The Coombs test is positive, uterine milk agglutinates calf RBCs and hemolysis occurs when complement is added. In moderate cases, PCV drops to 18% in the first week after birth and rises to 30 in the third. Anemia is normochromic and macrocytic.
Diagnosis is usually based on clinical findings of complex anemia in neonatal calves from dams that have been vaccinated from the blood. Reinforcement occurs by agglutination of adult and calf RBCs with colostral and maternal sera.
Blood transfusion is usually not performed due to incompatibility with the donor. A simple transfusion from an unvaccinated cow or a transfusion of saline-treated uterine RBCs may be helpful in increasing PCV to 25. Antibiotics and steroids may be helpful.
If there is any doubt, the disease can be predicted by establishing the presence of a titer against bovine RBC in cows. In practice, untitered cows' colostrum should be used until a positive doe has been milked for 24-48 hours.
Hemolytic diseases of newborn foals:
Affected foals are normal at birth but can absorb critical amounts of isoantibodies from the colostrum through their GJ tract within 36 hours. Clinically recognizable neonatal isoelectrolysis occurs less frequently in foals from primary porosity dams and is usually not detected until birth in a given womb of 3 or 4 foals. Uterus is isoimmunized naturally with focal placental rupture, which allows fetal placental hemorrhage of incompatible foal blood to contain a blood factor absent in the mother. Individual stallions bred to susceptible dams always produce susceptible foals due to the fact that they are genetically homozygous for the blood factor. Other stallions (heterozygous) rarely produce such foals, although neonatal erythrorhysis can occur in foals of any breed, most likely in mules and Thoroughbreds.
The severity of anemia varies greatly depending on the number and types of isoantibodies consumed. Hemolytic antibodies are the most damaging and the highest titers are found in the first dose of colostrum; consequently, vigorous foals that are poorly fed immediately after birth may be particularly affected.
