Anemia: causes, types, diagnosis, prevention. Anemia: causes and types, signs and manifestations, how to treat Consequences of anemia in older age

There can be several types of anemia, but the most common is iron deficiency. It is diagnosed in more than 80% of all cases and develops against the background of an acute lack of iron in the body. The microelement itself plays an important role in blood formation, so without it red blood cells and hemoglobin cannot be produced. The consequences of anemia also affect the production of cellular enzymes.

If malaise, general weakness, drowsiness, rapid heartbeat and other symptoms begin to occur, they should not be ignored and associated with ordinary fatigue. Failure to take timely measures to eliminate this pathology can lead to irreversible consequences for the body.

General possible consequences

Without proper treatment, the consequences of anemia can be quite serious:

  1. Enlargement of the liver with subsequent disturbances in its functioning.
  2. Deterioration immune system organism, leading to the development infectious pathologies. As a result, a person with anemia is more susceptible to viral and respiratory diseases.
  3. A decrease in concentration and intelligence occurs as a result of the fact that brain cells do not receive enough nutrition.
  4. Swelling of the lower extremities.
  5. Chronic fatigue, which reduces the functioning of all body functions and worsens the patient’s quality of life.
  6. Epithelial destruction. Cells of the skin and mucous membranes undergo deformation, which in turn leads to the development of gastrointestinal pathologies, as well as the appearance of eczema, erythema and other skin diseases.
  7. Disturbances in the functioning of the nervous system. Anemia also negatively affects this system, making a person more nervous, irritable, with sudden mood swings and other characteristic changes.
  8. The development of cardiopathy and heart failure, which can be fatal. If cells regularly do not receive enough oxygen, then the load on the heart increases and complications develop in its work.

Anemia is a fairly serious disease, which, in the absence of timely measures to eliminate it, can lead to irreversible complications.

Consequences of anemia in older age?

Anemia and its consequences are risk factors for many serious illnesses. With a regular lack of oxygen, as well as when enzymes are disrupted, the risk of developing cerebral ischemia, as well as cardiac tissue, increases. And by the age of 50, the onset of a stroke or heart attack is approaching. Anemia itself accelerates this process and has the following consequences:

  • Blockage of blood vessels with plaques;
  • Infarction of internal organs;
  • Closure of the lumen of large vessels.

In old age, a person who has anemia, in most cases already has foci of cardiosclerosis and serious disorders in his body heart rate. Also, against the background of anemia, liver function is disrupted at the cellular level, which entails various pathologies gastrointestinal tract.

There is a deterioration in the quality of food processing and absorption by the body medicines. This means that it is more difficult for the doctor to determine the dosage of medications. As a rule, by the age of 50 there are some chronic diseases, the treatment of which is complicated by the consequences of anemia.

Many cells in the body, including neurons in the brain, suffer from this lack of oxygen. This oxygen starvation contributes to early old age, memory impairment and decreased intellectual abilities. Without treatment, anemia can lead to serious complications and the development of chronic diseases.

Consequences of anemia for pregnant women

This disease can often develop during pregnancy. The last trimester is characterized by blood dilution, which is physiological in nature. However, if anemia occurs for more than early stages, then this is a reason to consult a doctor. Timely detection of pathology can take the necessary measures in time and reduce the risk of developing negative consequences, both for the mother and for her unborn child.

Even on early stage this pathology can increase the risk of developing preeclampsia (late toxicosis), as well as structural changes in the placenta itself. Against this background, the fetus experiences oxygen starvation, which can lead to a delay in its development, muscle atrophy and other negative factors.

Anemia can also cause serious complications of the birth process, namely:

  1. A protracted initial period, which occurs as a result of the slow opening of the uterus.
  2. Weak contractions and absence of labor.

You can reduce the risk of the negative effects of anemia during pregnancy by getting regular blood tests.

Consequences for the fetus

If anemia is detected in the mother, its effects can be passed on to the unborn child. A hypoxic state leads to disruption of the formation of the baby’s internal organs, and as a result, he is born with various defects.

Also, anemia often leads to premature birth. A premature baby, if rescued, is born with underdeveloped respiratory and digestive system. Nursing such children takes place in a special isolator under complete sterility and requires a lot of time and effort. The most dangerous consequence Anemia during pregnancy results in stillbirth.

As you can see, anemia is a pathology circulatory system which can cause serious complications. Its danger can be minimized with timely diagnosis. Therefore, you should not neglect annual medical examinations and turn a blind eye to the appearance of warning symptoms. Moreover, in the early stages, treatment consists of a special diet and giving up bad habits.

© Use of site materials only in agreement with the administration.

Human blood in its composition is a mixture of plasma (liquid base) and elementary solid particles represented by platelets, leukocytes and erythrocytes. In turn, platelets are responsible for coagulation, leukocytes maintain normal immunity, and red blood cells are oxygen carriers.

If for some reason the blood level () decreases, then this pathology is called anemia or anemia. General symptoms diseases manifest themselves in the form of pallor, weakness, dizziness, etc. As a result of anemia, an acute lack of oxygen begins in the tissues of our body.

Anemia is more often detected in women than in men. This pathology can occur against the background of any diseases, or develop as an independent disease.

Causes and general signs of anemia

Quite a few factors can provoke anemia. One of the most common causes of anemia is rightfully considered a lack of folic acid, or vitamin B12. Anemia also develops due to heavy bleeding during menstruation or against the background of certain cancer diseases. Often anemia occurs due to a deficiency of substances that are responsible for the production of hemoglobin, as well as disruptions in the formation of red blood cells. Inherited diseases and exposure to toxic substances can also cause the development of anemia.

The most common symptoms experienced by those suffering from anemia are:

  • Yellowish, flaky, cold to the touch and pale skin.
  • Weakness, fatigue, drowsiness and dizziness, in severe cases accompanied by fainting.
  • Low blood pressure.
  • Yellowish tint to the whites of the eyes.
  • Shortness of breath.
  • Weakened muscle tone.
  • Rapid heartbeat.
  • Enlargement of the spleen.
  • Changed stool color.
  • Sticky, cold sweat.
  • Vomiting, nausea.
  • Tingling in legs and arms.
  • Hair begins to fall out and nails break.
  • Frequent headaches.

Video: What is anemia and which parts of the body are affected?

Classification

In general, the classification of anemia is based on three groups:

  1. Posthemorrhagic anemia, i.e. anemia caused by severe.
  2. Anemia formed due to disturbances in the process of blood formation, as well as pathologies in the synthesis of RNA and DNA - megaloblastic, iron deficiency, folate deficiency, B-12 deficiency, hypoplastic, aplastic, Fanconi anemia and other types.
  3. Hemolytic anemias, i.e. anemia resulting from increased red blood cell destruction (autoimmune hemolytic anemia, sickle cell anemia, etc.).

In addition, anemia is divided into several degrees of severity, which depend on the hemoglobin content. This:

  • Severe degree - when there is less hemoglobin in the blood than 70 hl.
  • Average – 70-90 g/l.
  • Mild – more than 90 g/l (1st degree anemia).

Posthemorrhagic anemia

These types of anemia can be chronic or acute. Chronic, as a rule, is a consequence of repeated blood loss, for example, due to wounds and injuries, heavy menstruation, stomach ulcers, or cancer, etc. The acute form of posthemorrhagic anemia develops due to a single but significant blood loss.

At the same time, the clinical picture of acute posthemorrhagic anemia is represented by a significant deterioration in the patient’s general condition, associated with: rapid heartbeat, flashing “midges”, weakness, shortness of breath, tinnitus, dizziness, etc. The skin color becomes significantly paler, sometimes with a yellowish tint. The patient's general body temperature is reduced, the eye pupils are dilated.

An interesting fact is that a blood test performed within 2-3 hours after blood loss (with acute form posthemorrhagic anemia) shows normal levels of red blood cells and hemoglobin. Their rates begin to decline later. It is worth noting that the blood clots much faster.

The most effective way to treat posthemorrhagic anemia is considered. After which the doctor, as a rule, prescribes the patient to take antianemic drugs and a protein-enriched diet.

If the form is chronic, then, as a rule, the patient does not notice any special changes in the condition. Usually there is some pallor, dizziness when standing up suddenly and weakness. IN initial stages normal composition blood is provided by the bone marrow. Over time, it no longer copes with this function and develops hypochromic anemia. This is anemia, in which it is at a low level, which indicates a low hemoglobin content in red blood cells. The patient's nails begin to break and hair falls out.

In the chronic form of posthemorrhagic anemia, it becomes difficult for the iron to be absorbed in the body, which leads to significant disturbances associated with the formation of hemoglobin. The maximum effectiveness of treatment is achieved by neutralizing the source of blood loss.

In addition, iron supplements are prescribed. The most popular and effective medications for anemia in this case are: Ferroplex, Ferrum Lek, Conferon, Ferrocal, Feromide, etc. Treatment with iron-containing drugs proceeds quite for a long time. Doctors advise reconsidering the diet - it should be based on foods enriched with animal protein (meat, liver) and containing a lot of iron (buckwheat, apples, pomegranate).

Anemia developing against the background of blood formation disorders

Iron deficiency anemia

As a rule, iron deficiency anemia(IDA) develops due to a lack of an element such as iron in the body. This may be facilitated by various disorders associated with the absorption of iron, or the food consumed is poor in this element (for example, in those on a strict and long-term diet). IDA is also common in donors and people suffering from hormonal disorders.

In addition to the above, IDA can occur due to prolonged and heavy menstrual bleeding or cancer. Quite often, this anemia is diagnosed in pregnant women, since their needs for this element increase significantly during pregnancy. In general, IDA is most often found in children and women.

There are quite a few symptoms of iron deficiency anemia and they are often similar to the symptoms of other anemias:

  1. Firstly, the skin. It becomes dull, pale, flaky and dry (usually on the hands and face).
  2. Secondly, nails. They become brittle, dull, soft and begin to exfoliate.
  3. Thirdly, hair. In people with IDA, they become brittle, split, begin to fall out rapidly and grow slowly.
  4. Fourthly, teeth. One of characteristic features Iron deficiency anemia causes tooth staining and tooth decay. The enamel on the teeth becomes rough, and the teeth themselves lose their former shine.
  5. Often a sign of anemia is a disease, for example, atrophic gastritis, functional disorders of the intestines, genitourinary tract, etc.
  6. Patients with IDA suffer from taste and olfactory perversion. This manifests itself in the desire to eat clay, chalk, sand. Often such patients suddenly begin to like the smell of varnish, paint, acetone, gasoline, exhaust gases, etc.
  7. Iron deficiency anemia also affects general condition. It is accompanied by frequent pain in the head, rapid heartbeat, weakness, flashing “midges,” dizziness, and drowsiness.

A blood test for IDA shows a serious drop in hemoglobin. The level of red blood cells is also reduced, but to a lesser extent, since the anemia is hypochromic in nature (the color index tends to decrease). The iron content in the blood serum drops significantly. Siderocytes completely disappear from the peripheral blood.

Medicines for iron deficiency anemia

Treatment is based on taking iron-containing medications, both tablets and injections. Most often, the doctor prescribes iron supplements from the list below:

  • Ferrum-lek;
  • Ferrocal;
  • Ferkoven;
  • Ferramide;
  • Ferroplex;
  • Ferbitol;
  • Gemostimulin;
  • Imperon;
  • Conference, etc.

Diet for anemia

In addition to medications, doctors advise adhering to a certain diet associated with limiting flour, dairy and fatty foods. Healthy foods include buckwheat, potatoes, garlic, herbs, liver, meat, rose hips, currants, etc.

This anemia most often develops during pregnancy. Patients with IDA benefit from both forest and mountain air and physical exercise. It is advisable to use mineral water from Zheleznovodsk, Marcial and Uzhgorod sources. We should not forget about prevention in the autumn-spring periods, when the body is especially weakened. During these periods, a diet for anemia rich in iron-containing foods will be useful (see above and in the figure on the right).

Video: iron deficiency anemia - causes and treatment

Aplastic and hypoplastic anemia

These anemias are a complex of pathologies characterized by functional bone marrow failure. Aplastic anemia differs from hypoplastic anemia in that hematopoiesis is more depressed.

Most often, the occurrence of hypoplastic anemia is caused by radiation, certain infections, the negative effects of chemicals or drugs, or heredity. All possible forms Hypo- and aplastic anemias have a gradual development.

These anemias are manifested by fever, sore throat, sepsis, excess weight, pallor, and gum, pinpoint capillary hemorrhages on the mucous membranes and skin, and a burning sensation in the mouth. Often the disease is accompanied by complications of an infectious nature, for example, an abscess after an injection, pneumonia, etc.). The liver also often suffers - it usually becomes larger.

Iron metabolism in the body is disrupted, and the amount of iron in the blood is increased. There are much fewer leukocytes in the blood, as well as hemoglobin, but young forms of red blood cells are completely absent. Bloody impurities are often present in stool and urine.

In severe cases, aplastic anemia (like hypoplastic anemia) can be fatal. Treatment will give good results only if it is timely. It is carried out only in a hospital and implies increased hygienic care oral cavity and skin. This involves repeated blood transfusions, antibiotic therapy, taking vitamins and hormones, and also preferably good nutrition with anemia. Sometimes doctors resort to bone marrow transplantation (transfusion) (this is possible if there is a donor compatible with the HLA system, which requires special selection).

Fanconi anemia

This is a fairly rare type of congenital anemia associated with chromosomal abnormalities and defects in stem cells. Occurs preferentially in boys. In newborns, this pathology is usually not observed. It is characterized by symptomatic manifestations at 4-10 years of age in the form of bleeding and hemorrhage.

In the bone marrow, an increase in adipose tissue is observed, while cellularity is reduced, and hematopoiesis is suppressed. Studies show that in children with Fanconi anemia, red blood cells live ≈ 3 times less than normal.

The appearance of a patient with this anemia is characterized by abnormal pigmentation, short stature, underdevelopment of the skull or skeleton, and clubfoot. Often these symptoms are supplemented by mental retardation, strabismus, deafness, underdevelopment of the genital organs, kidneys, etc.

Blood tests show changes similar to aplastic anemia, only they are much less pronounced. Urinalysis in most patients shows high content it contains amino acids.

Fanconi anemia is a special case of aplastic anemia with impaired formation of red blood cells in the bone marrow

Patients with Fanconi anemia, according to studies, have a high predisposition to acute leukemia.

At its core , Fanconi anemia is a severe form of aplastic anemia described above. Treatment consists of removing the spleen, followed by the use of antilymphocyte globulin. Immunosuppressants and androgens are also used. But most effective treatment Bone marrow transplantation has proven itself (donors are the patient’s sister or brother or strangers who match the HLA phenotype).

This pathology has not yet been sufficiently studied. Although, despite its congenital nature, this anemia does not manifest itself in infants. If the disease is diagnosed late, then such patients do not live more than 5 years. Death occurs due to hemorrhages in the stomach or brain.

Megaloblastic anemias

These anemias are both hereditary and acquired. They are characterized by the presence of megaloblasts in the bone marrow. These are nucleated cells that are the precursors of red blood cells and contain non-condensed chromatin (in such a cell there is a young nucleus, but the cytoplasm surrounding it is already old).

Both B-12 deficiency and folate deficiency anemia are subtypes of megaloblastic anemia. Sometimes mixed B-12 folate deficiency anemia is even diagnosed, but it is quite rare.

B-12 deficiency anemia

B-12 deficiency anemia develops due to a lack of vitamin B-12. This trace element is necessary for proper functioning nervous system, and also it is needed bone marrow for the formation and growth of red blood cells in it. B-12 is directly involved in the synthesis of RNA and DNA, which is why the process of formation and development of red blood cells is disrupted when there is a shortage of it.

A distinctive feature is some unsteadiness in gait. The disease is also accompanied by heart pain, swelling of the limbs, weakness, reduced performance, pale jaundice and puffiness of the face, tinnitus, burning and itching on the tongue.

Typically, B-12 deficiency occurs due to impaired absorption. People with atrophy of the gastric mucosa, chronic enteritis, and celiac disease are more susceptible to this. B-12 deficiency can be a consequence of pancreatitis. It often occurs in vegetarians and older people.

This anemia is also called pernicious anemia. The disease develops very slowly, usually turning into a chronic relapsing form.

Treatment is carried out using parenteral vitamin B-12 (daily intramuscular injections). A diet enriched with B-12-containing foods is also indicated: liver, eggs, dairy products, meat, cheese, kidneys.

Folate deficiency anemia

Folate deficiency anemia is acute lack of folic acid in the body. She, too (like B-12) is actively involved in the formation of red blood cells. Folic acid is delivered to our body through food (meat, spinach, etc.), but when these products are thermally processed, it loses its activity.

This anemia often occurs in children fed goat's milk or powdered milk, and in pregnant women. In this case, the disease is accompanied by dizziness and weakness, shortness of breath and fatigue. The skin becomes dry and acquires a pale yellowish-lemon tint. The patient may often feel chills and fever.

Changes in the blood are identical to B-12 deficiency anemia. As a rule, hemoglobin remains normal, and sometimes even increased. The blood contains macrocytes - these are red blood cells that have an increased size. Folate deficiency anemia is generally characterized by a reduced number of all blood cells with an increase in their size. This is hyperchromic anemia with quite high rate colors. Blood biochemistry shows that it is slightly elevated.

Folate deficiency anemia is treated with folic acid medications in tablet form. In addition, the patient’s diet should be adjusted (leafy vegetables, liver, and more fruits are preferred).

Separately, it should be noted that B-12 and folate deficiency anemia are types of macrocytic anemia - this is a pathology characterized by an increase in the size of red blood cells due to an acute lack of B-12 or folic acid.

Hemolytic anemia

All varieties of these anemias are caused by excessive destruction of red blood cells. Normally, the lifespan of red blood cells is ≈120 days. When a person develops antibodies against his own red blood cells, a sharp destruction of red blood cells begins, i.e. the life of red blood cells becomes significantly shorter (≈13 days). Hemoglobin in the blood begins to break down, which is why the patient develops jaundice against the background of hemolytic anemia.

The laboratory symptom of such anemia is increased bilirubin, the presence of hemoglobin in the urine, etc.

Hereditary varieties occupy a significant place among such anemias. They are the consequences of many defects in the formation of red blood cells at the genetic level. Acquired varieties of hemolytic anemia develop against the background of certain factors that have a destructive effect on red blood cells (mechanical effects, various poisons, antibodies, etc.).

Sickle cell anemia

One of the most common hereditary hemolytic anemias is sickle cell anemia. This disease implies the presence of abnormal hemoglobin in red blood cells. This pathology most often affects African Americans, but it also occurs in fair-skinned people.

The presence of sickle-shaped red blood cells in the blood, characteristic of this pathology, usually does not threaten its carrier. But if both mother and father have this pathological hemoglobin in their blood, then their children risk being born with a severe form of sickle cell anemia, which is why such anemia is dangerous.

photo: blood for hemolytic anemia. Red blood cells are irregularly shaped

This type of anemia is accompanied by rheumatic pain, weakness, pain in the abdomen and head, drowsiness, swelling of the legs, hands and feet. A medical examination reveals pallor of the mucous membranes and skin, an enlarged spleen and liver. People with this pathology are characterized by a thin physique, tall stature and a curved spine.

A blood test shows a moderate or severe degree of anemia, and the color indicator will be normal.

This pathology is a serious disease. The majority of patients die, as a rule, before reaching the age of ten, due to some kind of infection (usually tuberculosis) or internal hemorrhage.

Treatment of this anemia is symptomatic. Although it is considered chronic anemia, children can easily tolerate low levels of red blood cells and hemoglobin. That is why they rarely receive blood transfusions (more often in cases of aplastic or hemolytic crisis). All kinds of infections should be avoided, especially for children.

Autoimmune hemolytic anemia

Among acquired varieties, autoimmune hemolytic anemia is more common. It involves the influence of antibodies formed in the patient’s body. This type occurs, as a rule, in chronic cirrhosis and hepatitis, rheumatoid arthritis, acute leukemia, or chronic lymphocytic leukemia.

There are chronic as well as acute forms of autoimmune hemolytic anemia. The chronic form proceeds practically without characteristic symptoms. In the acute form, the patient suffers from jaundice, shortness of breath, weakness, fever, rapid heartbeat. Feces Due to the excessive content of stercobilin, they have a dark brown tint.

Although rare, autoimmune anemia with complete cold antibodies can be found, which is characteristic of older people. Cold in such cases acts as a provoking factor, leading to swelling and blue discoloration of the fingers, face, and feet. Often autoimmune anemia of this type is accompanied by Raynaud's syndrome, which, unfortunately, can result in gangrene of the fingers. In addition, in patients with cold autoimmune anemia impossible to determine using traditional methods.

Treatment is carried out using glucocorticoid hormones. An important role in treatment is played by its duration and the correct dosage of drugs. Also in treatment, doctors use cytostatic drugs, perform plasmapheresis, and, if necessary, splenectomy.

Video: anemia in the program “Live Healthy!”

It should be remembered that many types of anemia, if treated incorrectly, can have severe consequences for the body, including death. Therefore, there is no need to self-medicate. The diagnosis must be made by a qualified doctor, as well as effective and correct treatment must be prescribed!

Anemia of the brain and its membranes (Anemia cerebri et meningum) is a disease characterized by a decrease in blood flow to the brain, as a result of which the body develops a disorder of brain function and oxygen starvation of brain tissue.

Animals of all types are affected, but horses are most common.

Etiology. Anemia of the brain and its membranes most often occurs in animals as a secondary disease, with large blood losses, pronounced cardiac vascular insufficiency(with complete atrioventricular heart block, acute dilatation of the heart, arterial hypotension), compression of the carotid artery area by a harness, or sudden outflow of a large amount of blood to internal organs, for example, after the rapid release of transudate during dropsy or fermenting gases by a trocar during and swelling of the cecum in horses, with a drop in intra-abdominal pressure during rapid labor. Anemia of the brain in animals can occur with decreased vascular tone and decreased blood pressure with traumatic shock, with arteriosclerosis of cerebral vessels, acute infectious diseases and intoxications.

Chronic anemia of the brain and membranes in animals is observed when there is difficulty in blood flow in the cranial cavity due to increased intracranial pressure (symptomatic anemia with hydrocephalus, brain tumors), with myocardial dystrophy, cardiac fibrosis, decompensated heart defects, with hypoplastic anemia, infectious anemia, leukemia, disorders metabolism, vitamin deficiencies.

Pathogenesis. As a result of decreased blood flow to the brain, malnutrition occurs nerve tissue. Brain cells need a continuous supply of glucose and oxygen. With an insufficient supply of glucose and oxygen, as a result of a decrease in the reserves of high-energy compounds, accumulation of under-oxidized metabolic products occurs in the nerve cells: lactic acid, carbon dioxide, inorganic phosphate, glycogen, etc., a weakening of the processes of excitation and inhibition in the brain, which leads to nervous distortion -reflex activity, weakening in animals muscle tone, disorders of secretion and motility of the stomach and intestines, disorders of pulmonary and tissue gas exchange.

Clinical picture. With acute anemia of the brain in animals, rapidly progressing symptoms of dysfunction of the cortex and subcortical centers are observed. Animals develop depression, disorder of consciousness, general weakness and loss of coordination of movements. In severe cases of the disease, a sick animal may develop a fainting or comatose state, in such cases the animal falls to the ground and loses “consciousness.” Against the background of a comatose state, the animal may die.

For chronic anemia The brain is characterized by a slow increase in dysfunction of the cortex and subcortical centers: decreased reaction to the environment, lethargy, apathy, soporous or stuporous state, decreased muscle tone, loss of coordination of movements, fibrillary muscle contractions. In cattle, atony of the forestomach and weakened intestinal motility are observed.

In acute and chronic anemia of the brain, symptoms of cardiovascular failure are almost always observed: pallor with a bluish tint of visible mucous membranes, low-fill pulse, arrhythmias, dullness of heart sounds, decreased maximum blood pressure and an increase in minimum, increased venous pressure.

The duration of the disease depends on the causes that caused it. In mild cases, the sick animal quickly recovers, but the resulting depression and lethargy, atony of the forestomach and decreased productivity may remain for a long time.

Forecast careful. The outcome of an animal’s disease depends on the timeliness of care medical care and the nature of etiological factors. Progressive weakness, the disappearance of the animal's pupillary response to light, the appearance of convulsions, abnormal weak breathing and deterioration in the quality of the pulse should serve as a signal of an unfavorable prognosis for the veterinarian.

Pathological changes. The vessels of the meninges are weakly filled with blood, the choroid plexuses are poorly distinguishable, and the membranes themselves are pale. The brain is pale, the boundary between the gray and white matter of the cerebral cortex is smoothed.

Differential diagnosis. We differentiate from acute, hypomagnesemia, coma in various diseases.

The prognosis in acute cases of the disease, subject to timely provision of medical care, is favorable. In chronic anemia, the prognosis ranges from questionable to unfavorable.

Treatment begin by giving the animal rest, placing the head as low as possible. Further treatment carried out depending on the reasons that caused brain anemia. In case of bleeding, measures are taken to stop it immediately, a 10% calcium chloride solution is injected intravenously, and to replenish the blood volume, saline is injected intravenously or a homogeneous blood transfusion is performed. For anemia caused by blood redistribution, vigorous rubbing of the skin with tourniquets is carried out, rubbed into the skin of the lateral surfaces chest or stomach turpentine or mustard alcohol, inhale ammonia, rub ammonia near the ears, monitor the work of the heart and breathing. When the heart weakens, the animal is given caffeine, camphor, cordiamine, corglycon, and oxygen inhalation is prescribed. Korglikon is given intravenously to animals in the form of a 0.06% solution in the following doses: horses 4-5 ml; cows 3-8ml; dogs 0.5 -1 ml; Korglykon is administered in a 40% glucose solution. Cordiamine is administered subcutaneously to horses and cattle. 10-20ml; pigs 1-4ml; dogs 0.5-2ml. In more severe cases, aminophylline and other vasoconstrictors are used to eliminate cerebral apoplexy. medicines. In the chronic course of the disease, in order to improve the functioning of the heart and metabolic processes in the brain, a course of cardiac glucosides, B vitamins, Cerebrolysin, aminolon, and piracet is prescribed. In cases where the cause of brain anemia is a tumor, high-value animals undergo surgery. Sick animals must be kept in well-ventilated areas (to partially compensate for insufficient blood circulation with oxygen) and provided with adequate protein and vitamin composition diet. Recovered animals are gradually brought into work.

Prevention. Prevention of brain anemia involves early diagnosis and treatment of diseases that lead to vascular insufficiency (posthemorrhagic anemia, heart defects, diabetes mellitus, cardiomyopathy). Animal owners must follow the rules for adjusting harnesses for working animals (collars, yokes, etc.), collars for dogs, and avoid excessive exploitation of animals. Carry out timely treatment for blood loss. Follow the rules when puncturing the scar (tympany), slowly release gases and liquids during punctures of the peritoneal cavity.

Anemia of the brain and its membranes(anaemia cerebri et meningum)

Anemia of the brain and its membranes - a disease characterized by a decrease in blood flow to the brain, a deterioration in its nutrition and a violation of the functional state.

Etiology. Anemia of the brain and its membranes often occurs as a secondary disease, complicating the course of many disease processes. In acute cases, the disease can develop as a result of redistribution of blood during its outflow to the organs abdominal cavity, for example, with a sharp drop in intra-abdominal pressure due to the rapid removal of a large amount of gases through the trocar during scar tympany, during rapid labor. Anemia of the brain occurs when vascular tone decreases and blood pressure decreases during traumatic shock, acute infectious diseases and intoxication. Less commonly, brain anemia occurs after heavy external or internal bleeding.

Chronic anemia of the brain is noted when there is difficulty in blood flow in the cranial cavity due to increased intracranial pressure (symptomatic anemia with hydrocephalus, brain tumors), with hypoplastic anemia, myocardial dystrophies, heart valve defects (narrowing of the aortic opening).

Pathogenesis. As a result of a decrease in blood flow to the brain, the nutrition of the nervous tissue is disrupted. Brain cells need a continuous supply of glucose and oxygen. With a lack of glucose and oxygen, the reserves of high-energy compounds are reduced, and biosynthetic processes are disrupted. In nerve cells, under-oxidized metabolic products accumulate: lactic acid, carbon dioxide, inorganic phosphate, glycogen, etc. Perversion of metabolic processes leads to the disappearance of the excitability of nerve cells and the development of internal inhibition in them, which is manifested by characteristic symptoms.

Sometimes the distortion of metabolic processes in nerve cells is accompanied by their excitation, but a progressive lack of oxygen and glucose ultimately leads to the depletion of nerve cells and the disappearance of their excitability.

Symptoms. Acute anemia of the brain is characterized by symptoms indicating a decrease in the excitability of nerve cells: depression, disturbance of consciousness, weakness, locomotor and static ataxia. Reflexes weaken and disappear. The pupil is dilated and does not respond to light. The mucous membranes are pale. The pulse is rapid, weak, of small filling, often thread-like. The heartbeat is pounding at first, then weak. Breathing is rapid, shallow, and often irregular. With anemia caused by bleeding, a coma quickly occurs. Seizures and convulsions are rarely observed. The duration of the disease depends on the causes that caused it. In mild cases, the animal recovers quickly, but depression, lethargy, atony of the forestomach, and decreased lactation can remain for a long time. In severe cases, the disease leads to the death of the animal.

With chronic anemia, the same symptoms are noted, but they are less pronounced: fatigue, depression, weakened reflexes, fearfulness, ataxia, fibrillary contractions, cramps and convulsions of individual muscle groups, rumen atony, weakened intestinal motility. Changes in the cardiovascular system and respiration are similar to those in acute anemia of the brain. In a lying animal, the symptoms of brain anemia weaken, which is taken into account when making a diagnosis.

The forecast is cautious. The outcome of the disease depends on the timeliness of medical care and the nature of the etiological factors. Progressive weakness, disappearance of the pupil's reaction to light, the appearance of convulsions, irregular weak breathing and deterioration in the quality of the pulse make the prognosis unfavorable.

Pathological and anatomical changes. The vessels of the meninges are weakly filled with blood, the choroid plexuses are poorly distinguishable, and the membranes themselves are pale. The brain is pale, the border between the cortex and white matter is smoothed.

Treatment begins with providing rest, giving the animal’s head the lowest possible position. Further treatment is carried out differentially depending on the causes of brain anemia.

For anemia caused by blood redistribution, vigorous rubbing of the skin with tourniquets, inhalation of ammonia, and monitoring of heart function and breathing are performed. When the heart weakens, caffeine, camphor are injected, and oxygen inhalation is prescribed. In more severe cases, aminophylline and other vasodilators are used to eliminate cerebral apoplexy.

Rp.: Sol. Euphyllini 12% - 2.0 D.t.d. N 2 in ampullis
S.: Cow. Intravenously. For one injection, dilute in 200 ml of 40% glucose solution.

In case of anemia of the brain resulting from blood loss, stop the bleeding. Calcium chloride and blood replacement fluids are administered intravenously.

Rp.: Sol. Calcii chloridi sterilisate 10% -200.0 D.S.: Cow. Intravenously. For one injection.

In case of chronic anemia of the brain, the underlying disease is identified and eliminated, the diet is improved, and good zoohygienic conditions for keeping animals are provided.

Prevention of nutritional anemia, in particular cerebral anemia, consists of complete, balanced feeding of animals, inclusion in the diet of microelements necessary for normal hematopoiesis, and circulatory anemia - in the timely stop of bleeding, compliance with the rules of puncture of the scar during tympany.

In case of chronic anemia of the brain, the underlying disease is identified and eliminated, the diet is improved, and good zoo-hygienic conditions are provided.

A disease characterized by weakening of the function of the cerebral cortex due to insufficient blood circulation in the vessels of the brain and its membranes. All types of animals are affected, but horses and dogs are more common. It occurs in acute and chronic forms.
Etiology. Most common cause primary acute anemia of the brain is an insufficient flow of arterial blood to the brain, which is observed with bleeding, severe cardiovascular failure, accompanied by complete atrioventricular heart block, acute dilatation of the ventricles, arterial hypotension, compression of the carotid artery area with a harness, sudden redistribution of blood (with rapid removal gases from the rumen, stomach and intestines) or removal of exudates and transudates from the abdominal cavity during puncture. Secondary acute anemia is possible with traumatic shock, bruises, and injuries.
Chronic anemia develops as a result of damage to hematopoiesis, leukemia, increased intracranial pressure, dropsy and brain tumors, narrowing of the aortic opening and insufficiency of its valves, as well as myocardosis, myocardial fibrosis and traumatic pericarditis.
Pathogenesis. As a result of insufficient influx of oxygen and nutrients (glucose) with arterial blood in the nerve cells of the brain, the processes of excitation and inhibition are disrupted, which leads to distortion of neuro-reflex activity, weakening of muscle tone, disorders of secretion and motility of the stomach and intestines, disorders of the pulmonary and tissue gas exchange.
Symptoms. With acute anemia, general weakness, unsteadiness of gait, progressive depression, weakening or loss of conditioned reflexes develop, and the animal may fall to the ground. During fainting, the activity of the heart is weak, the arterial pulse is small, thread-like, frequent, breathing is slow, deep or, conversely, rapid, superficial. Visible mucous membranes are pale, the pupils are dilated. Sometimes yawning and vomiting are observed, which is more common in carnivores.
Chronic anemia is manifested by lethargy, apathy, decreased tone skeletal muscles, ataxia, stupor, less often a soporotic state (continuous deep sleep with loss of reaction to the environment). Sometimes clinical signs of brain damage are not observed, which is a consequence of the brain’s adaptability to impaired blood circulation.
Pathomorphological changes. The vessels of the meninges are poorly filled with blood, the membranes are anemic, the brain is pale, the border between the cortex and the white matter is smoothed.
Diagnosis and differential diagnosis. Diagnosed on the basis of anamnesis and characteristic clinical signs(depression, drowsiness, coma). Ophthalmoscopy reveals pallor of the optic papilla and anemia of the fundus.
Forecast. In acute cases of the disease, subject to timely provision of medical care, favorable, in chronic anemia - from doubtful to unfavorable.
Treatment. First of all, the causes of the disease are eliminated. For anemia caused by blood redistribution, vigorous rubbing of the skin with tourniquets and short-term inhalations of ammonia are performed. Hot compresses are placed on the head and copious cold enemas are given. To stimulate the heart, caffeine, camphor are injected, and oxygen inhalations are prescribed. In case of posthemorrhagic anemia, measures are taken to stop bleeding. Hemostatic agents are administered intravenously (10% solution of calcium chloride or gluconate intravenously - horses and cows 100-300 ml, dogs 5-10 ml; sodium etamsylate, vikasol, etc.), as well as blood-substituting fluids (polyglucin, reopoliglucin, reoglu- man, rheogem, rheomacrodex). Sick animals are kept in ventilated rooms and provided with a nutritious diet. The recovered animals are gradually brought back into work.
Prevention. Follow the rules for fitting harnesses for working animals and collars for dogs. Timely treatment of bleeding is necessary. When puncturing the proventriculus and abdominal cavity, gases and liquids should be released slowly.

Share: