Diseases

Iron deficiency types of anemia account for almost 80% of all cases of this disease. These include posthemorrhagic anemia, which is considered one of the most frequently diagnosed. This disease occurs due to severe blood loss. This disease can have either an acute form or develop into a difficult-to-diagnose chronic form. In the first case, posthemorrhagic develops due to a sudden appearance heavy blood loss. The chronic form appears with frequent but small internal bleeding.

Hemorrhagic anemia

This disease develops rapidly and poses a real danger to human life. Acute hemorrhagic anemia can be fatal. Therefore, when such a problem occurs, the patient should urgently seek medical help. A one-time loss of 500 ml of blood is considered critical. The chronic form of the disease can significantly worsen a person’s quality of life. Constant, but not heavy bleeding also often indicates the development of various cardiological, gynecological and gastroenterological problems.

Symptoms of diseases

Signs of chronic and acute forms of the disease can vary greatly. With regular, but not heavy bleeding the patient appears faintly severe symptoms. He may complain about:

• pale skin;
• fatigue;
• loss of performance;
• dizziness;
• darkening of the eyes;
• decrease in body temperature.

Posthemorrhagic anemia the acute type causes more obvious symptoms. It is important to know how to identify excessive internal blood loss in order to immediately call medical care. In this condition, the patient experiences:

A sign of internal bleeding is dry mouth. The person may also experience nausea, vomiting, and confusion. The problem can also be indicated feces. When internal bleeding occurs, they turn black. Against the background of general intoxication of the body, the patient’s body temperature may increase. The patient also complains of a feeling of compression of the internal organs. The greater the blood loss, the more clearly the above symptoms appear.

The appearance of this disease is always associated with a lack of blood in the body. Acute posthemorrhagic anemia occurs most often due to injuries, during which damage to blood vessels and large arteries occurs. In addition, the disease can appear when:

• surgical interventions;
• rupture fallopian tube with ectopic pregnancy;
• peptic ulcer stomach and duodenum;
• severe lung diseases;
• violation of hemostasis.

An acute form of anemia occurs with massive blood loss, which can be caused by damage to the walls of the heart chambers during a heart attack. The disease also often develops when an aortic aneurysm ruptures. This disease can also appear in infants. Their problem is associated with birth injuries, as well as placental bleeding.

The chronic form of hemorrhagic anemia manifests itself with the loss of small volumes of blood associated with various gastrointestinal, renal, hemorrhoidal and nasal injuries. The problem may appear when uterine bleeding, gingivitis, hemorrhoids and intestinal tumors.

In women, this disease can occur with very heavy menstruation, dysmenorrhea. Sometimes this disease is diagnosed in pregnant women. Their anemia may be associated with serious pathologies. For example, the problem may occur when:

• umbilical cord rupture;
• placental abruption;
• choriangioma;
• hematoma of the placenta.

If a person experiences symptoms of acute posthemorrhagic anemia, then emergency medical assistance must be urgently called. The faster the resuscitation team arrives, the higher the likelihood successful treatment. Doctors such as:

A patient who is experiencing symptoms chronic anemia, should seek help from these specialists. He may also need to undergo consultations with a hematologist, gastroenterologist, gynecologist, or proctologist. At the first appointment, the doctor must carefully listen to all the patient’s complaints. The doctor will definitely examine the patient and also ask him a few clarifying questions:

1. When did you first notice symptoms of the disease?
2. Have there been similar problems in the past?
3. Are you worried about chronic diseases?
4. Are there any other health complaints?
5. Are you taking any medications?

The survey allows the specialist to compile a complete clinical picture diseases. It also helps to find the true root cause of the development of posthemorrhagic anemia. The doctor must refer the patient for examination to confirm the diagnosis. The patient will have to take a general and biochemical tests blood, which will determine the lack of hemoglobin. Ultrasound, ECG, radiography and FGS are performed to determine the cause of internal bleeding.

Features of treatment

Therapy may vary significantly depending on what form of anemia the patient has. If a person is diagnosed with acute hemorrhagic anemia, he is urgently hospitalized. All efforts of doctors will be aimed at immediately eliminating bleeding. To do this they can:

• carry out dressing;
• perform suturing of blood vessels;
• increase blood clotting;
• carry out resection and suturing of damaged organs.

In the future, hemorrhagic anemia may not require any treatment, since the body will begin to actively restore the lost amount of blood. This is performed by activating blood depots, which are located in the liver, lungs, and spleen.

If the patient has lost a lot of blood, then he needs an urgent transfusion. At severe conditions The patient may also be given:

• blood replacement solutions;
• B vitamins;
• electrolyte solutions;
• iron supplements.

The prognosis for this disease depends on how quickly the person received qualified medical care. With prolonged and heavy bleeding, acute posthemorrhagic anemia can provoke hypovolemic shock, after which the patient can fall into a coma.

Treatment of posthemorrhagic anemia

Therapy for chronic anemia also begins with finding and eliminating the cause of bleeding. Having eliminated this problem, doctors prescribe to the patient drug treatment. It consists of taking one of the following medications.

Posthemorrhagic anemia is a pathology that in medicine belongs to the category of iron deficiency. The cause of its development may be a severe injury with significant bleeding or the presence of a lesion in the body chronic blood loss. Posthemorrhagic anemia can be acute or chronic. The acute form of posthemorrhagic anemia is an option in which the pathology develops against the background of heavy bleeding, while chronic form- this is the result of systematic, but not heavy bleeding.

In the presence of bleeding in the body, a rapid decrease in the volume of circulating blood and, first of all, its plasma is observed. Accordingly, there is a sharp drop in the level of red blood cells, which leads to the development of acute hypoxia and then anemia, which belongs to the group of post-hemorrhagic.

Symptoms

When collecting complaints and anamnesis, the doctor receives the following clinical picture: the patient experiences weakness of the body, strong and frequent dizziness, which can reach fainting. Also, with posthemorrhagic anemia, nausea is observed, and in the acute form of the condition, vomiting may occur. During the course of pathology in the body, trophic disorders, accordingly, structural pathological changes occur skin, hair and nails.

At this option anemia, shortness of breath, angina-type heart pain, and muscle weakness can often be observed. Patients quite often complain of dry mouth and difficult to quench thirst, flashing spots before the eyes, and tinnitus. Also included in the clinical picture of this type of anemia is a sharp decline body temperature.

With heavy bleeding, symptoms may develop hemorrhagic shock.

Diagnostics

The presence of posthemorrhagic anemia can only be determined using laboratory methods blood tests. When diagnosing, it is also worth taking into account the patient’s medical history, complaints and results. instrumental studies, which determine the location of the source of bleeding. To the number instrumental methods diagnostics in this case include fibrogastroduodenoscopy and colonoscopy.

Prevention

First of all, you need to try to avoid the disease of posthemorrhagic anemia, therefore, you should avoid as much as possible any injuries that can cause blood loss and bleeding.

Prevention of the development of posthemorrhagic anemia also includes healthy image life and observance proper nutrition, in which the blood and all body systems receive the required amount of microelements and vitamins. The diet must contain iron-containing foods, namely, fresh fruits, lean red meat, legumes, fresh green vegetables, whole grain bread and herbs.

Treatment

The first stage of treatment for posthemorrhagic anemia is aimed at eliminating the source of bleeding and preventing state of shock. Next, you need to carry out treatment aimed at replenishing lost blood, while heparin must be replenished in the body and the level of red blood cells must be normalized. Thus, the volume of replenished blood should not exceed 3/5 of the volume of lost blood; the remaining deficit is replenished with the help of blood substitutes.

At the third stage of therapy, after stopping bleeding, blood loss is restored, and nothing threatens life, curative therapy with help iron-containing preparations and vitamin complexes.

After eliminating the symptoms of anemia, treatment with iron-containing drugs continues for another 6 months, but the amount taken medicines reduced by half.

Etiology

Acute posthemorrhagic anemia characterized by rapid loss of hemoglobin and red blood cells in the blood and appears as a result of bleeding.

Anemia is based on a decrease in the mass of circulating red blood cells, leading to impaired oxygenation of body tissues.

Pathogenesis

Hypovolemia is accompanied by stimulation of the sympathetic-adrenal system. Redistribution reactions develop at the level of the capillary network, resulting in phenomena of intravascular aggregation shaped elements blood. Disruption of capillary blood flow leads to the development of hypoxia of tissues and organs, the filling of under-oxidized and pathological metabolic products and intoxication, venous return decreases, which leads to a decrease in cardiac output. Decompensation of microcirculation occurs, caused by a combination of vascular spasm with aggregation of red blood cells, which creates conditions for the formation of blood clots. From the moment signs of erythrocyte aggregation form, shock becomes irreversible.

Clinic of acute posthemorrhagic anemia

The clinical picture depends on the amount of blood lost, the duration of bleeding and the source of blood loss.

Acute phase - after blood loss, the leading clinical manifestations are hemodynamic disorders (decreased blood pressure, tachycardia, pallor of the skin, loss of coordination, the development of shock, loss of consciousness)

Reflex-vascular phase, after blood loss, there is a compensatory flow of blood deposited in the muscles, liver, spleen into the bloodstream

Hydraemic phase of compensation, which lasts 1-2 days after bleeding, while anemia is detected in blood tests

Bone marrow stage of blood loss compensation, 4-5 days after blood loss develops reticulocyte crisis, which is characterized by: reticulocytosis, leukocytosis.

After day 7, the blood loss recovery phase begins, if bleeding does not recur, then after 2-3 weeks the red blood is completely restored, and there are no signs of iron deficiency anemia.

Diagnosis of posthemorrhagic anemia

Blood test: decrease in NV, number of red blood cells, it is normochromic, normocytic, regenerative - reticulocytes more than 1%

Treatment of acute posthemorrhagic anemia:

Treatment of acute posthemorrhagic anemia begins with stopping bleeding and anti-shock measures. In order to improve capillary blood flow, the bcc in the body should be replenished; influence the physical and chemical properties of blood. In case of severe blood loss, transfusion saline solutions, maintaining the electrolyte balance of the body. The prognosis depends on the rate of blood loss - a rapid loss of up to 25% of the total blood volume can lead to the development of shock, and a slow blood loss even within 75% of the total body weight can end favorably!

IRON-DEFICIENCY ANEMIA

IDA is a clinical and hematological syndrome, which is based on a violation of hemoglobin synthesis, due to iron deficiency in the body or due to a negative balance of this microelement for a long time.

There are three stages in the development of iron deficiency:

Pre-latent iron deficiency or decreased iron stores.

Latent iron deficiency is characterized by depletion of iron in the depot, but the concentration of HB in peripheral blood remains above the lower limit of normal. Clinical symptoms at this stage are little expressed, manifested by a decrease in tolerance to physical activity.

Iron deficiency anemia develops when the concentration of HB drops below physiological values.

Etiological factors of IDA

IDA is the most common anemia; it occurs in 10-30% of the adult population of Ukraine. The reasons for the development of this pathology are: malnutrition, diseases of the digestive tract, accompanied by chronic blood loss and impaired iron absorption (hemorrhoids and rectal fissures, gastritis, gastric ulcer, etc.) Diseases of the genitourinary system, complicated by micro- and macrohematuria (chronic glomerulus - and pyelonephritis, polyposis Bladder etc.) Increased need for iron: pregnancy, lactation, uncontrolled donation, frequent inflammation.

Pathogenesis of IDA

Iron is a very important trace element in the human body; it takes part in oxygen transport, redox and immunobiological reactions. Insufficient amount of iron for the body is replenished with food. For normal absorption of dietary iron, free hydrochloric acid is necessary in the stomach, which converts it into an oxidized form, the latter in the small intestine binds to the protein apoferetin, forming ferretin, which is absorbed into the blood.

Iron, which appears during the destruction of red blood cells in the spleen (from heme), is included in the composition of feretin and hemosiderin (reserve iron) and also partially enters the bone marrow and is used by erythroblasts.

Iron contained in the body can be divided into functional (as part of hemoglobin, myoglobin, enzymes and coenzymes), transport (transferin), deposited (ferritin, hemosiderin) and iron, which forms a free pool. Of the iron contained in the body (3-4.5 mg), only 1 mg is involved in the exchange with external environment: excreted in feces, lost during hair loss, cell destruction.

The daily iron requirement of an adult in a state of physiological equilibrium is (1 - 1.5) mg, for women during menstruation - (2.5 - 3.3) mg.

Clinical picture of IDA

Except ANEMIC SYNDROME IDA is also typical SIDEROPENIC SYNDROME, which is associated with a violation of the trophism of epithelial cells as a result of a decrease in the activity of iron-containing enzymes - cytochromes. It manifests itself changes in the skin and its appendages– the skin becomes dry, sluggish, turgor decreases, nails become brittle, hair loss appears, the perception of smells and taste changes – an addiction to the smell of gasoline, chalk, acetone, etc. arises. Changes in mucous membranes gastrointestinal tract cheilitis, angular stomatitis, tendency to periodantosis, dysphagia (Plumer-Vinson syndrome), atrophic gastritis. Happening atrophy of the mucous membranes of the eyes in the form of dryness eyeball, “blue sclera symptom”, changes in the mucous membranes of the upper and lower respiratory tract, Atrophic rhinitis, pharyngitis, and bronchitis develop. The muscular system is affected - growth and physical development are delayed, muscle weakness, weakening of the muscular apparatus of the sphincters - imperative urge to urinate, nocturnal anuresis, etc.

Diagnosticsiron deficiency anemia

General blood analysis– decrease in NV, number of red blood cells, hypochromia, anisocyto-, poikilocytosis, microcytosis.

Blood chemistry

Decreased iron content in blood serum

Increase in the total iron-binding capacity of blood serum

Decrease in ferritin and transferrin levels

Treatment of iron deficiency anemia: identification and elimination of the cause of the development of IDA; correction of iron deficiency by prescribing iron-containing drugs for internal use.

Principles of treatment with iron supplements:

Dietary iron does not correct iron deficiency.

Preference is given to drugs containing ferrous iron.

Avoid taking nutrients which reduce iron absorption ( calcium supplements, cottage cheese, milk, tannin in tea).

It is not advisable to simultaneously prescribe B vitamins and folic acid, if there is no concomitant anemia.

Treatment for 12 months after normalization of HB levels in maintenance doses to replenish iron reserves;

Parenteral iron supplements are prescribed only in cases of malabsorption due to intestinal pathology, exacerbation of peptic ulcer disease, intolerance to oral iron supplements, and the need to quickly saturate the body with iron.

Megaloblastic anemias

(due to deficiency of vitamin B12 and folic acid)

B12-(folate)-deficiency anemia is a group of anemias in which there is a violation of DNA and RNA synthesis, which leads to impaired hematopoiesis, the appearance of megaloblasts in the bone marrow, and the destruction of erythrokaryocytes in the bone marrow.

Etiology of B12 and folic anemias

Vitamin B12 deficiency can develop due to malabsorption. This is due to a decrease in the secretion of the internal factor of Castle (patients after gastrectomy, type A gastritis).

Damage to the small intestine (celiac disease, blind loop syndrome, multiple diverticulosis, small intestine).

With competitive absorption of large amounts of vitamin B12 in the intestines (diphyllobothriasis).

Sometimes, but not often, exogenous vitamin B12 deficiency can occur (vitamin deficiency in foods or prolonged heat treatment of foods).

The causes of folate deficiency anemia are most often associated with the use of folic acid antagonists (methotrxate, acyclovir, triamterene), chronic alcoholism, malnutrition, and diseases of the small intestine.

Pathogenesis

Vitamin B12 deficiency leads to a lack of the coenzyme methylcobolamine, which in turn affects DNA synthesis, hematopoiesis is disrupted, and atrophy of the mucous membranes of the gastrointestinal tract occurs. With this anemia, the activity of the coenzyme deoxyadenosylcobolamine decreases, which leads to impaired fatty acid metabolism, accumulation of methyl malonate and propionate, which causes damage to the nervous system and the development of funcular myelosis.

Folic acid deficiency leads to ineffective hematopoiesis with a shortened life expectancy of not only red blood cells, but also other nucleated cells (hemolysis and cytolysis of granulocytes, platelets), a decrease in the number of red blood cells and, to a lesser extent, hemoglobin, leukopenia, neutropenia, thrombocytopenia, as well as changes in the functioning of some organs and systems of the body.

ClinicB12 and folate deficiency anemia

In B12 and folate deficiency anemia, damage occurs nervous system, funicular myelosis develops (demyelization of nerve endings) - parasthesia appears, the sensitivity of the limbs is impaired, and spastic spinal paralysis appears.

Changes in Gastrointestinal tract manifest themselves in the form of dyspeptic syndrome (diarrhea, bloating, rumbling, nausea, loss of appetite), the mucous membranes are affected - a burning sensation of the tongue, the mucous membrane of the mouth and rectum, a “varnished” tongue with areas of inflammation - Hunter’s glossitis, loss of taste occurs

Mental disorders– hallucinations, depressive syndrome, unsteady gait, impaired tactile and temperature sensitivity, Skin changes– pale skin with a lemon-yellow tint (moderate anemia), subecteric sclera

Possible moderate hepatosplenomegaly – liver enlargement and

spleen

DiagnosticsB12 deficiency anemia

Blood analysis: decrease in the amount of hemoglobin and red blood cells, macrocytic, hyperchromic anemia, basophilic punctuation of red blood cells is detected, which is more characteristic of B12 anemia (Jolly bodies, Cabot rings);

Bone marrow: erythroid hyperplasia with characteristic megaloblastic type of hematopoiesis in the bone marrow (“blue bone marrow”);

Treatment

Important in the treatment of these anemias is elimination of the etiological factor and therapeutic nutrition: a sufficient amount of meat, liver, milk, cheese, eggs.

TreatmentB12 deficiency anemia:

Vit preparations At 12 for parenteral administration

cyanocobalamin, hydroxycobalamin

Course treatment: 400-500 mcg/day. IM during the first two weeks; then 400-500 mcg after 1-2 days until red blood counts normalize.

If there are signs of funicular myelosis, a course of treatment of 1000 mcg/day. until all neurological symptoms disappear.

Treatmentfole deficiency anemia

Folic acid is prescribed at a dose of 3-5 mg/day until clinical remission is achieved. Pregnant women are prescribed a prophylactic dose of 1 mg/day. An indicator of effectiveness is a reticulocyte crisis on days 6-7 from the start of treatment and the presence of a normoblastic type of hematopoiesis, with the gradual onset of complete clinical and hematological remission.

HEMOLYTIC ANEMIA

Hemolytic anemia- a group of anemias, which is characterized by a decrease in the average life expectancy of red blood cells, which is due to their increased destruction and accumulation of red blood cell breakdown products - bilirubin - in the blood and the appearance of hemosiderin in the urine.

Etiology of hemolytic anemias –

Hereditary hemolytic anemias may be associated with a violation of the structure of the erythrocyte membrane; caused by impaired activity of erythrocyte enzymes, impaired structure or synthesis of hemoglobin.

Pathogenesis

The normal lifespan of red blood cells is 100-120 days. It is important to say that anemia develops if the compensatory capabilities of erythropoiesis lag behind the rate of destruction of red blood cells.

With hemolytic anemia, the lifespan of red blood cells can be reduced to 12 days. This increases the activity of free bilirubin, which has a toxic effect on body tissues, and hemosiderin, which can be deposited during internal organs and lead to hemosiderosis. At the same time, the amount of urobilin in the urine and stercobilin in the feces increases. With hemolytic anemia, a tendency to form stones in the gall bladder often develops due to the increased content of bilirubin in the bile.

Clinic

Hemolysis is characterized by a triad : jaundice, splenomegaly, anemia of varying severity. The severity of jaundice depends on the degree of destruction of red blood cells on the one hand and on the functional ability of the liver to bind bilirubin because Jaundice appears against the background of anemia, then the skin becomes lemon yellow. With hemolytic anemia, cholelithiasis can develop and, as complications, cholestatic hepatitis and cirrhosis of the liver.

The appearance of hemolytic anemia leads to impaired physical and mental development.

Hereditary anemia, in particular microspherocytosis, can be manifested by hypoplastic crises: a drop in hemoglobin levels, an increase in the concentration of indirect bilirubin, reticulocytosis, increased jaundice, fever, abdominal pain, and weakness.

Diagnosis of anemia

Blood analysis: decrease in NV, number of red blood cells, normochromic anemia, reticulocytosis, number of leukocytes and platelets does not change, leukocytosis is possible only after a crisis. The osmotic resistance of red blood cells may be reduced (hereditary ovalocytosis).

To exclude hereditary hemolytic anemia, it is necessary to identify the morphology of erythrocytes (spherocytosis, ovalocytosis, elliptocytosis).

Carrying out a genetic analysis - all anemias associated with a defect in protein membranes are inherited by the dominant type, and enzymopathies by the recessive type.

Biochemical analysis blood: increased amount bilirubin due to indirect, increasing the amount of iron. Urobilin is detected in urine, stercobilin is detected in feces.

In autoimmune hemolytic anemia, a positive Coombs test is detected, and antibodies to red blood cells are detected.

Bone marrow: red hyperplasia bone marrow due to erythrokaryocytes.

Treatment

Treatment of hemolytic anemia depends on the pathogenesis of the disease.

For autoimmune hemolytic anemia Pathogenetic therapy is prescribed - corticosteriids; if they are ineffective, patients can receive cytostatic drugs such as cyclophosphamide or azathioprine. Treatment is usually carried out in combination with prednisolone. Persons with G-6-FDG deficiency should be prohibited from taking “oxidative” drugs (sulfonamides, antimalarials, sulfones, analgesics, chemicals, nitrofurans).

Red blood cell transfusions are prescribed only in cases of severe enzyme deficiency. Measures are needed to improve diuresis in hemoglobinuria. Splenectomy is performed only for strict indications:

Severe course of the disease with functional impairment;

If cholecystectomy is necessary, splenectomy must be performed simultaneously.

Due to increased destruction of red blood cells, folic acid must be included in therapy.

(HYPO)-APLASTIC ANEMIA

Aplastic anemia is characterized by profound inhibition of bone marrow hematopoiesis and pancytopenia, which causes the main manifestations of the disease.

According to the etiological factor, they distinguish:

Acquired forms (exposure to chemical and physical agents, medications, toxins, viruses).

Idiopathic forms.

Hereditary forms (Fanconi anemia, hereditary deficiency of pancreatic hormones, hereditary dyskeratosis)

Clinichypo-aplastic anemia

For aplastic anemia with damage to three layers of hematopoiesis, the following syndromes are characteristic: anemic, hemorrhagic, immunodeficiency and febrile.

Hemorrhagic syndrome due to inhibition of the platelet layer, manifests itself in the form of rashes of the petichial-spot type, hemorrhages throughout the body, bleeding from the nose, uterus, gastrointestinal and others. Immunodeficiency syndrome manifests itself due to inhibition of leukocyte activity and a decrease in the body's immune resistance. This is manifested by frequent colds: sore throats, bronchitis, pneumonia. Feverish syndrome is characterized by an increase in temperature to subfebrile levels, weakness, and chills.

Diagnosis of hypo-aplastic anemia

General blood analysis- normochromic anemia, moderate anisocytosis and poikilocytosis, reduced reticulocyte count, leukocytopenia, thrombopenia

Biochemical analysis blood: serum iron concentration is increased. Determination of the renal complex, bilirubin and its fractions (hemolytic and anemia associated with impaired regulation of erythropoiesis). Immune disorders: autoantibodies to blood and bone marrow cells, auto- and allosensitization in 35% of patients, inhibition of the phagocytic reaction of neutrophils.

Bone marrow: inhibition of hematopoietic germs, hypocellularity with relative lymphocytosis in the classic type of acquired aplastic anemia.

Treatment:

Mode: Cancel all medicines, to which there is individual hypersensitivity.

Drug treatment:

1. Hemostatic therapy: corticosteroids - prednisolone 60-80 mg, dexamethasone, polcortalone.

2. Anabolic steroids (especially after splenectomy): retabolil, nerobolil, methandrostenolone.

3. Replacement therapy:

transfusion of washed red blood cells (for severe anemia);

platelet transfusion (for hemorrhages).

4. Antilymphocyte globulin (rabbit and goat - intravenously 120-160 mg 10-15 times).

5. Antibiotic therapy for infectious complications.

Surgical treatment: bone marrow transplant, removal of an organ that produces antibodies - splenectomy

Posthemorrhagic anemia - iron deficiency anemia, which develops after blood loss. Fast hemorrhagic anemia develop as a result of the loss of a significant amount of blood into the external environment or into the body cavity. The leading pathogenetic link of these anemias is a decrease in the speed and total volume of blood, especially its circulating fraction, which leads to hypoxia, shifts in the acid-base state, and an imbalance of ions in and outside the cells. Depending on the rate of blood loss, acute (develops after heavy, acute bleeding) and chronic posthemorrhagic anemia (develops after prolonged, light bleeding) are distinguished.

Etiology

• hemorrhagic diseases (thrombocytopathies, coagulopathy, disseminated intravascular coagulation syndrome, hemorrhagic vasculitis, leukemia, aplastic anemia, dysovarian menorrhagia in girls).

  pulmonary hemorrhage, gastrointestinal bleeding

Pathogenesis

With rapid blood loss, the volume of circulating blood decreases (oligemic phase). In response to a decrease in the volume of circulating blood, a compensatory reaction occurs: excitation of the sympathetic nervous system and reflex vascular spasm, arterial-venous shunting, which initially helps maintain blood pressure, adequate venous inflow and cardiac output. The pulse is accelerated and weakened. The vessels in the skin and muscles are narrowed to the maximum, the vessels of the brain and coronary vessels are minimally narrowed, which ensures better blood supply to vital organs. As the process continues, the phenomena of posthemorrhagic shock begin.

Clinic

With posthemorrhagic anemia, clinically, the phenomena of acute vascular insufficiency due to sudden emptying of the vascular bed (hypovolemia) come to the fore: palpitations, shortness of breath, orthostatic collapse). The severity of the condition is determined not only by the quantity, but also by the rate of blood loss. There is a decrease in diuresis according to the degree of blood loss. Hemoglobin level and red blood cell count are not reliable indicators of the degree of blood loss.

In the first minutes, the Hb content may even be high due to a decrease in bcc. When tissue fluid enters the vascular bed, these indicators decrease even when bleeding stops. The color index, as a rule, is normal, since there is a simultaneous loss of both red blood cells and iron, that is, normochromic anemia. On the second day, the number of reticulocytes increases, reaching a maximum on days 4–7, that is, the anemia is hyperregenerative.

Diagnostics

In the diagnosis of posthemorrhagic anemia, information about acute blood loss that occurred due to external bleeding is taken into account; in the case of massive internal bleeding, the diagnosis is based on clinical signs in combination with laboratory tests (Gregersen, Weber), an increase in the level of residual nitrogen in bleeding from the upper gastrointestinal tract.

With external bleeding, the diagnosis is easy to make. In case of internal bleeding from an organ, collapse of another origin must be excluded.

Treatment

The most important thing is to eliminate the source of bleeding. Then the blood loss is replaced (depending on the severity of anemia - red blood cells, against the background of heparin administration). The total volume of blood transfusion should not exceed 60% of the deficit in circulating blood volume. The remaining volume is filled with blood substitutes (5% albumin solution, rheopolyglucin, Ringer's solution, etc.). The limit of hemodilution is considered to be a hematocrit of 30 and red blood cells of more than 3*10¹²/l. At the end of the acute period, treatment with iron supplements and vitamins B, C, E is necessary. After anemia is eliminated, iron supplements are prescribed in half the dose for up to 6 months.

Forecast

The prognosis depends on the cause of bleeding, speed, volume of blood loss, and rational therapy. With blood loss with a deficit of circulating blood volume of more than 50%, the prognosis is unfavorable.

Acute posthemorrhagic anemia

They develop as a result of injuries accompanied by a violation of the integrity of blood vessels, bleeding from internal organs, more often with damage to the gastrointestinal tract, uterus, lungs, heart cavities, after acute blood loss due to complications of pregnancy and childbirth. The larger the caliber of the affected vessel and the closer to the heart it is located, the more life-threatening the bleeding. Thus, when the aortic arch ruptures, it is enough to lose less than 1 liter of blood for death to occur due to a sharp drop in blood pressure and a deficiency in filling the cavities of the heart. Death in such cases occurs before bleeding of the organs occurs, and during autopsy of the corpses of the deceased, anemia of the organs is hardly noticeable. With bleeding from small vessels, death usually occurs when more than half of the blood is lost. total number blood. If the bleeding turns out to be non-fatal, then the blood loss is compensated by regenerative processes in the bone marrow. With acute blood loss (1000 ml or more) within a short time, signs of collapse and shock come first. Anemia begins to be detected hematologically only 1-2 days after blood loss, when the stage of hydremic compensation develops. In the first hours after acute blood loss, a decrease in blood clotting time can serve as a reliable indicator.

Clinical picture such anemia is characterized by pallor of the skin and visible mucous membranes, weakness, dizziness, tinnitus, cold sticky sweat, a sharp decrease in blood pressure and body temperature, blurred vision up to complete amaurosis (specific elements of the retina are very sensitive to anoxemia), frequent pulse of weak filling (thread-like), agitation, followed by fainting, sometimes vomiting, cyanosis, convulsions. A significant amount of iron is lost (500 mg or more). If blood loss is not quickly replaced, collapse (shock), decreased diuresis, anuria occur, and renal failure develops. As a result of a sharp decrease in the mass of red blood cells, the respiratory function of the blood decreases and oxygen starvation develops - hypoxia. Particularly sensitive in this regard nervous system and sense organs.

Clinical picture in acute blood loss depends on the volume of blood lost, speed, and duration of bleeding. The severity of such anemia, especially in the initial stages of formation, is largely determined by a decrease in circulating blood volume (CBV). Based on this feature, the following degrees of blood loss are distinguished:

moderate blood loss - up to 30% of blood volume;

massive blood loss - up to 50% of the blood volume;

severe blood loss - up to 60% of blood volume;

fatal blood loss - over 60% of the blood volume.

For acute posthemorrhagic anemia, the following stages are distinguished:

Reflex-vascular stage, which develops in the first hours after blood loss, is characterized by a proportional decrease in the mass of erythrocytes and plasma. Blood pressure drops sharply, pallor of the skin and mucous membranes develops, tachycardia and tachypnea occur. Hypovolemia and hypoxia, occurring immediately after blood loss, activate the sympathoadrenal system, which leads to spasm peripheral vessels, the opening of arteriovenular shunts and the release of blood from the organs that deposit it. Those. The compensatory reaction of the body is reduced to bringing the volume of the vascular bed in line with the volume of circulating blood due to reflex vascular spasm, which prevents a further drop in blood pressure and helps maintain adequate venous return of blood to the heart. In the reflex-vascular stage, the content of erythrocytes, hemoglobin, and leukocytes practically does not change, since the total amount of blood decreases, and changes do not have time to occur in each unit of its volume. The hematocrit does not change either. This is due to the fact that during blood loss, equivalent volumes of plasma and red blood cells are simultaneously lost. Thus, despite the clear clinical picture, anemia during this period does not have any hematological manifestations and is hidden, latent in nature.

Hydremic stage develops in the next 3-5 hours (depending on blood loss), the volume of circulating blood is restored due to the entry of interstitial interstitial fluid into the vascular bed. Irritation of volume receptors due to hypovolemia triggers a standard reflex reaction aimed at maintaining a constant volume of circulating blood. The body increases the production of renin, angiotensin II, and aldosterone. An increase in aldosterone synthesis leads to sodium retention, and subsequently, through stimulation of ADH secretion, to water retention. All this leads to an increase in blood volume, but due to blood thinning, the number of red blood cells and hemoglobin per unit volume decreases. Simultaneously with the mobilization of tissue fluid into the blood, the production of plasma proteins by the liver increases. Protein deficiency is restored in 3-4 days. Anemia at this stage is normochromic. Phenomena of aniso- and poikilocytosis (pathological deviations in the size and shape of red blood cells) may be observed. The color index remains normal due to the fact that mature red blood cells that were in the vascular bed before blood loss circulate in the blood. The hematocrit begins to decrease and is extremely low numbers reaches 48-72 hours after blood loss, because the plasma volume is restored by this time, and the maturation of erythrocytes is delayed. As for leukocytes and platelets, in the immediate hours after blood loss, redistribution leukocytosis and posthemorrhagic thrombocytosis can be observed due to the release of the deposited parietal pool of leukocytes and platelets into the blood. However, as hemodilution progresses, the number of leukocytes and platelets per unit volume of blood begins to decrease. The platelet content may also fall due to their consumption during the process of thrombus formation. The stage of hydremic compensation can last 2-3 days.

Bone marrow stage develops on the second and subsequent days (usually from 4-5 days), and as hypoxia progresses, it is characterized by activation of erythropoiesis. Detected big number young cells of the erythrocyte germ of hematopoiesis: polychromatophilic and oxyphilic erythrocytes. Increased proliferation of the erythroid germ causes an increase in reticulocytes in the blood, up to normoblasts. In mature erythrocytes circulating in the blood, morphological changes are detected - the appearance of anisocytes and poikilocytes, because acceleration of the entry of red blood cells into the blood is ensured by a jump through the stages of division. Red blood cells cannot be saturated with hemoglobin (hypochromia, i.e. color index below 0.85), since blood loss has led to loss of iron. Thrombocytosis and moderate neutrophilic leukocytosis develop with a regenerative shift to the left. Bone marrow cells of squamous and epiphyses tubular bones proliferate, the bone marrow becomes juicy and bright. Normalization of blood counts usually occurs after 3-4 weeks.

An example of a hemogram of a patient with acute posthemorrhagic anemia in the hydremic stage:

erythrocytes - 2.1·1012/l;

hemoglobin - 60 g/l;

color index - 0.86;

reticulocytes - 0.7%;

hematocrit - 0.19 l/l;

• anisocytosis +;

  ESR - 16 mm/h;

  platelets - 250·109/l;

  leukocytes - 5.0·109/l;

  eosinophils - 1%;

  basophils - 0%;

  neutrophils:

• stab - 3%;

  segmented - 54%

  lymphocytes - 38%;

  monocytes - 1%

Hemogram of the same patient, who is in the bone marrow stage of acute posthemorrhagic anemia:

erythrocytes - 3.6·1012/l;

hemoglobin - 95 g/l;

color index - 0.79;

reticulocytes - 9.3%;

hematocrit - 0.30 l/l;

• anisocytosis +;

  poikilocytosis +;

  polychromatophilia, single normocytes

  ESR - 21 mm/h;

  platelets - 430·109/l;

  leukocytes - 17.0·109/l;

  eosinophils - 1%;

  basophils - 0%;

  neutrophils:

• stab - 19%;

segmented - 58%

lymphocytes - 11%;

monocytes - 2%

During treatment In acute posthemorrhagic anemia, priority measures include stopping bleeding and combating shock, and then restoring blood composition. Transfusion and replacement therapy. The patient is given a blood transfusion, blood substitutes such as polyglucin, albumin solution, and saline solutions are administered, their volume depends on the amount of blood loss. Poliglyukin- a good plasma substitute, retained in the vascular bed for several days, ensuring stability of the circulating blood volume. Reopoliglyukin - the best remedy prevention and treatment of microcirculation disorders, reduces blood viscosity, causes disaggregation of erythrocytes and platelets, preventing thrombus formation. Indications for whole blood transfusion are only very massive blood losses. Due to the fact that blood loss is accompanied by adrenal insufficiency, it is necessary to administer corticosteroid hormones. After removing the patient from a serious condition, antianemic drugs are prescribed (iron supplements, a diet rich in proteins, vitamins, bioelements). In certain cases, surgery is indicated- ligation of a bleeding vessel, suturing of an ulcer, resection of the stomach, removal of a pregnant fallopian tube, etc. For bleeding that occurs with symptoms painful shock, it is necessary first of all to strive to bring the body out of a state of shock. Along with the administration of morphine and cardiovascular drugs (strychnine, caffeine, strophanthin, etc.), intravenous infusion of polyglucin, plasma (regular or hypertonic) or other anti-shock fluids is indicated. An infusion of hypertonic plasma (160 ml) should also be carried out as an emergency measure so that in the future, at the first opportunity, a whole blood transfusion can be performed. The effectiveness of plasma infusions is determined by the content of hydrophilic colloids in it- proteins, which ensure its isotonicity in relation to the recipient’s plasma, which contributes to a long-term retention of transfused plasma in the recipient’s vascular system. This is the undeniable advantage of plasma infusions over saline infusions, the so-called saline solution. The latter, when administered intravenously even in large quantities (up to 1 liter), is essentially ballast, since it almost does not linger in the bloodstream. Particular caution should be given to the practice of subcutaneous infusion of saline solution, which does not have any effect on disrupted hemodynamics and only leads to tissue edema.

Forecast depends on the duration of bleeding, the volume of lost blood, the body’s compensatory processes and the regenerative capacity of the bone marrow. A known difficulty is the diagnosis of the underlying disease in the case of bleeding from an internal organ, for example, during an ectopic pregnancy. In these cases, the syndrome of acute anemia, supported by a laboratory blood test, serves as a guiding thread that leads the doctor to the correct diagnostic path. The prognosis of acute posthemorrhagic anemia (in the first moments) depends not only on the amount of blood loss, but also on the rate of blood flow. The most extensive blood losses, even the loss of 3/4 of all circulating blood, do not lead to death if they occur slowly over a number of days. On the contrary, a rapid loss of 1/4 of the blood volume causes a state of dangerous shock, and a sudden loss of half the blood volume is certainly incompatible with life. A drop in blood pressure below a critical figure (70-80 mm for systolic pressure) can be fatal due to developing collapse and hypoxia. As soon as normal blood supply to the vessels is restored due to tissue fluid, the prognosis for life becomes favorable (if re-bleeding does not occur). The time frame for restoring a normal blood picture after a single blood loss is very different and depends both on the magnitude of the blood loss itself and on individual characteristics, in particular on the regenerative ability of the bone marrow and the iron content in the body. If we take the amount of iron in the erythrocyte mass of the body to be 36 mg per 1 kg of body weight, then if, for example, 30% of the erythrocyte mass is lost, the body will lose 10.8 mg of iron per 1 kg. If we take the monthly intake of alimentary iron into the body as equal to 2 mg per 1 kg, then the restoration of normal iron content, and therefore hemoglobin, will occur within approximately 5.5-6 months. Persons who are weakened or anemic even before blood loss, even after a single small bleeding, become anemic for a longer period. Only vigorous therapy can bring their hematopoietic organs out of the torpid state and eliminate anemia.

Chronic posthemorrhagic anemia

They are a particular variant of iron deficiency anemia. They are associated with increasing iron deficiency in the body due to either a single but heavy blood loss, or minor but prolonged, often repeated bleeding as a result of rupture of the walls of blood vessels (with the infiltration of tumor cells into them, venous stagnation of blood, extramedullary hematopoiesis, gingivitis, ulcerative processes in the wall of the stomach, intestines, skin, subcutaneous tissue, cancer), endocrinopathies (dishormonal amenorrhea), with renal, uterine bleeding, hemostasis disorders (disturbance of its vascular, platelet, coagulation mechanisms during hemorrhagic diathesis). They lead to depletion of iron reserves in the body and a decrease in the regenerative capacity of the bone marrow. Often the source of bleeding is so minor that it goes unrecognized. To imagine how small blood losses can contribute to the development of significant anemia, it is enough to cite the following data: the daily amount of dietary iron required to maintain hemoglobin balance in the body is about 5 mg for an adult. This amount of iron is contained in 10 ml of blood. Consequently, the daily loss of 2-3 teaspoons of blood during defecation not only deprives the body of its daily need for iron, but over time leads to a significant depletion of the body’s “iron fund,” resulting in the development of severe iron deficiency anemia. All other things being equal, the easier the development of anemia will be, the less iron reserves in the body and the greater (in total) blood loss.

Clinic . The complaints of patients are mainly reduced to severe weakness, frequent dizziness and usually correspond to the degree of anemia. Sometimes, however, one is struck by the discrepancy between subjective state the patient and his appearance. The patient's appearance is very characteristic: sharp pallor with a waxy tint to the skin, bloodless mucous membranes of the lips, conjunctiva, puffy face, weakness, fatigue, ringing or noise in the ears, dizziness, shortness of breath, the lower extremities are pasty, sometimes general edema (anasarca) develops due to hydremia and hypoproteinemia. As a rule, patients with anemia are not malnourished, unless the malnutrition is caused by an underlying disease (stomach or intestinal cancer). Anemic heart murmurs are observed (palpitations even with slight physical exertion), most often a systolic murmur is heard at the apex, conducted to the pulmonary artery, and a “topping noise” is noted on the jugular veins.

Blood picture characterized by hypochromia, microcytosis, low color index (0.6 - 0.4), morphological changes in erythrocytes - anisocytosis, poikilocytosis, polychromasia; the appearance of degenerative forms of erythrocytes - microcytes and schizocytes; Leukopenia is characteristic (if there are no special moments contributing to the development of leukocytosis), a shift of the neutrophil series to the left and relative lymphocytosis, the platelet count is normal or slightly reduced. The number of reticulocytes depends on the regenerative capacity of the bone marrow, which is greatly reduced by depletion of stored iron. The next phase of the disease is characterized by a decline in the hematopoietic activity of the bone marrow - anemia takes on a hyporegenerative character. At the same time, along with the progressive development of anemia, an increase in the color index is observed, which approaches one; anisocytosis and anisochromia are observed in the blood: along with pale microcytes, more intensely colored macrocytes are found. The blood serum of patients with chronic posthemorrhagic anemia is pale in color due to the reduced bilirubin content (which indicates reduced blood breakdown).

Bone marrow of flat bones of normal appearance. In the bone marrow of tubular bones, the phenomena of regeneration and transformation of fatty bone marrow into red, expressed to varying degrees, are observed. Multiple foci of extramarrow hematopoiesis are often observed. Due to chronic blood loss, hypoxia tissues and organs, which causes the development of fatty degeneration of the myocardium (“tiger heart”), liver, kidneys, and dystrophic changes in brain cells. Multiple pinpoint hemorrhages appear in the serous and mucous membranes and in the internal organs.

Rice. 4. Blood in chronic posthemorrhagic anemia: 1 and 2 - schizocytes; 3 - segmented neutrophils; 4 - lymphocyte; 5 - platelets.

According to severity anemia may be

moderate severity (hemoglobin content from 90 to 70 g/l)

Bone marrow hematopoiesis In acute cases, previously healthy individuals often experience a normal physiological reaction to blood loss with the production of first immature, polychromatophilic elements, and then mature, fully hemoglobinized red blood cells. In cases of repeated bleeding, leading to depletion of the body’s “iron fund,” a violation of erythropoiesis is noted in the phase of hemoglobinization of normoblasts. As a result, some cells die without having time to bloom, or enter the peripheral blood in the form of sharply hypochromic poikilocytes and microcytes. Subsequently, as anemia becomes chronic, the initial intensity of erythropoiesis decreases and is replaced by a picture of its inhibition. Morphologically, this is expressed in the fact that the processes of division and differentiation of erythronormoblasts are disrupted, as a result of which erythropoiesis takes on a macronormoblastic character. The described functional disorders of hematopoiesis are reversible, since we are talking about a hyporegenerative (not hypoplastic) state of the bone marrow.

Treatment includes most early detection and eliminating the cause of blood loss, for example, excision of hemorrhoids, gastric resection for a bleeding ulcer, extirpation of a fibromatous uterus, etc. However, a radical cure of the underlying disease is not always possible (for example, with inoperable gastric cancer). As well as replenishing iron deficiency (iron supplements are recommended for 2 - 3 or more months under the control of erythrocyte hemoglobin and iron content in the blood serum). To stimulate erythropoiesis, as well as as replacement therapy, it is necessary to perform repeated blood transfusions, preferably in the form of red blood cell transfusions. The dosage and frequency of blood (packed red blood cell) transfusions vary depending on individual conditions, but are mainly determined by the degree of anemia and the effectiveness of therapy. With a moderate degree of anemia, medium-dose transfusions are recommended: 200-250 ml of whole blood or 125-150 ml of red blood cells with an interval of 5-6 days. In case of sudden anemia of the patient, blood transfusions are performed in higher dosages: 400-500 ml of whole blood or 200-250 ml of red blood cells with an interval of 3-4 days.

Hematopoiesis and blood destruction in posthemorrhagic anemia.

Acute posthemorrhagic anemia

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Posthemorrhagic anemia - a set pathological changes, which develop in the body due to the loss of a certain amount of blood: it contains iron, and with blood loss it becomes insufficient. It is divided into two types: acute and chronic.

ICD-10 code

Chronic posthemorrhagic anemia has the following ICD-10 code - D50.0, and acute - D62. These disorders are located in the section “Anemia associated with nutrition. Iron-deficiency anemia".

Latin defines the word anemia as “lack of blood,” literally speaking. The word can also be translated as “anemia,” which means a lack of hemoglobin. And “hemorrhagic” is translated as “accompanied by bleeding,” the prefix “post” means “after.”

Information about what posthemorrhagic anemia is will allow you to detect its development in time and provide the necessary assistance.

Pathogenesis in posthemorrhagic anemia

Pathogenesis is a certain sequence of development of pathological changes, which makes it possible to judge the features of the occurrence of posthemorrhagic anemia.

The severity of posthemorrhagic anemia is determined by the hemoglobin content and the severity of tissue hypoxia due to its deficiency, but the symptoms of anemia and its features are associated not only with this indicator, but also with others that decrease with blood loss:

• Iron content;
• Potassium;
• Magnesium;
• Copper.

Particularly negative on circulatory system affected by iron deficiency, in which the production of new blood cells is difficult.

The minimum volume of blood that can be lost without the risk of developing serious disorders is 500 ml.

Donors donate blood without exceeding this amount. Healthy body a person with sufficient body weight completely restores the lost elements over time.

When there is not enough blood, small vessels constrict to compensate for the shortage and maintain blood pressure at normal level.

Due to a lack of venous blood, the heart muscle begins to work more actively to maintain sufficient minute blood flow - the amount of blood that is ejected by the heart per minute.

What colour deoxygenated blood can be read.

Read what the heart muscle consists of

The functioning of the heart muscle is impaired due to mineral deficiency, the heart rate decreases, and the pulse weakens.

An arteriovenous shunt (fistula) occurs between the veins and arterioles, and blood flows through the anastomoses without touching the capillaries, which leads to impaired blood circulation in the skin, muscular system, fabrics.

Formation of an arteriovenous shunt, due to which blood does not flow to the capillaries

This system exists to maintain blood flow to the brain and heart, allowing them to continue to function even in the face of severe blood loss.

Interstitial fluid quickly compensates for the lack of plasma (the liquid part of the blood), but microcirculation disturbances persist. If blood pressure drops significantly, blood flow speed will small vessels will decrease, which will lead to thrombosis.

In the severe stage of posthemorrhagic anemia, small blood clots form that clog small vessels, which leads to disruption of the functioning of the arterial glomeruli in the kidney tissue: they do not filter fluid properly, and the amount of urine excreted is reduced, and harmful substances are retained in the body.

Blood circulation in the liver also weakens. If you don't start timely treatment acute posthemorrhagic anemia, this will lead to liver failure.

With posthemorrhagic anemia, the liver suffers due to lack of blood

Oxygen deficiency in tissues leads to the accumulation of under-oxidized elements that poison the brain.

Acidosis develops: violation acid-base balance towards the predominance of an acidic environment. If posthemorrhagic anemia is severe, the amount of alkalis is reduced, and the symptoms of acidosis increase.

With blood loss, the level of platelets decreases, but this has little effect on the coagulation processes: the content of other substances that affect coagulation reflexively increases.

Over time, the clotting mechanisms return to normal, but there is a risk of developing thrombohemorrhagic syndrome.

Causes

The main factor influencing the development of posthemorrhagic anemia is blood loss, the causes of which can be different.

Acute posthemorrhagic anemia

This is a disorder that develops rapidly due to excessive blood loss. This dangerous condition, which requires the rapid initiation of treatment measures.

Causes of acute anemia:

Chronic posthemorrhagic anemia

A condition that develops with systematic blood loss over a long period of time. It can go unnoticed for a long time if the blood loss is mild.

Causes of chronic anemia:

Hemorrhagic anemia also develops due to vitamin C deficiency.

Kinds

Posthemorrhagic anemia is divided not only by the nature of its course (acute or chronic), but also by other criteria.

The severity of anemia is assessed by the amount of hemoglobin in the blood.

Depending on its content, anemia is divided into:

• Light. With mild anemia, hemoglobin begins to lack iron, its production is impaired, but the symptoms of anemia are practically absent. Hemoglobin does not fall below 90 g/l.
• Average. Symptoms when medium degree severity is moderate, hemoglobin concentration is 70-90 g/l.
• Heavy. In severe cases there are serious violations organ function, heart failure develops, the structure of hair, teeth, and nails changes. Hemoglobin content is 50-70 g/l.
• Extremely severe. If the hemoglobin level is below 50 g/l, there is a risk of life.

There are also individual pathologies included in the ICD:

• Congenital anemia in the newborn and fetus due to blood loss (code P61.3);
• Posthemorrhagic anemia chronic type, which is secondary iron deficiency (code D50.0).

Symptoms

Acute form of anemia

Symptoms in the acute form of posthemorrhagic anemia increase very quickly and depend on the severity of blood loss.

Observed:

A decrease in blood pressure due to massive blood loss is called hemorrhagic shock. The intensity of the fall in blood pressure depends on the severity of blood loss.

The following symptoms are also present:

• Tachycardia;
• The skin is cold and pale, with moderate and severe degrees it has a cyanotic (bluish) color;
• Impaired consciousness (stupor, coma, loss of consciousness);
• Weak pulse (if the stage is severe, it can only be felt on the main vessels);
• Reducing the amount of urine excreted.

The symptoms of posthemorrhagic anemia and hemorrhagic shock are joined by signs that are inherent to the disease that caused blood loss:

• With an ulcer, black or red stool is observed;
• Swelling in the impact area (if injured);
• When the arteries in the lungs rupture, there is a cough with bright scarlet blood;
• Intense bloody discharge from the genitals during uterine bleeding.

The source of bleeding is identified by indirect signs depending on the clinical picture.

Stages of acute posthemorrhagic syndrome

Spicy posthemorrhagic syndrome has three stages of development.

Name	Description
Reflex-vascular stage	The level of plasma and red blood cells drops, compensatory processes are activated, blood pressure drops, and the heart rate increases.
Hydremia stage	It develops several hours after blood loss and lasts from 2 to 3 days. Intercellular fluid restores the volume of fluid in the vessels. The content of red blood cells and hemoglobin decreases.
Bone marrow stage	Develops 4-5 days after blood loss due to oxygen starvation. The level of hematopoietin and reticulocytes, the precursor cells of red blood cells, increases in the blood. The amount of iron in the plasma decreases.

The body fully recovers after blood loss after two to three or more months.

Signs of chronic form

Chronic bleeding gradually leads to posthemorrhagic anemia, which develops gradually, and its symptoms are closely related to the severity of hemoglobin deficiency.

Observed:

People with posthemorrhagic anemia have low immunity and often develop infectious diseases.

Diagnostics

In case of acute blood loss, the patient remains on inpatient treatment so that risks can be assessed and timely assistance provided.

Laboratory diagnosis of posthemorrhagic anemia is carried out repeatedly, and the results vary depending on the stage and severity of the disorder.

Laboratory signs of acute anemia:

• In the first two hours, the concentration of platelets increases, and red blood cells and hemoglobin remain at normal levels;
• After 2-4 hours, the excess platelets remain, neutrophil granulocytes grow in the blood, the concentration of red blood cells and hemoglobin decreases, color index anemia is defined as normochromic (normal value);
• After 5 days, an increase in reticulocytes is noted, the iron level is insufficient.

What tests need to be taken?

Must be passed general analysis blood, in chronic anemia it reveals the content of elliptocytes, lymphocytes are increased in peripheral blood, but reduced in overall cellular composition.

A deficiency of iron, calcium, and copper is detected. Increased manganese content.

At the same time, tests are carried out to determine the cause of bleeding: stool examination for helminthiasis and occult blood, colonoscopy, urinalysis, bone marrow examination, ultrasonography, esophagogastroduodenoscopy, electrocardiogram.

Who to contact?

Hematologist

Treatment

Acute hemorrhagic anemia at the first stage of treatment requires eliminating the cause of blood loss and restoring normal blood volume.

Surgeries are performed to suture wounds and blood vessels, and the following medications are prescribed:

• Artificial blood substitutes. They are infused by drop or stream, depending on the patient’s condition;
• When shock develops, the use of steroids (Prednisolone) is indicated;
• Soda solution eliminates acidosis;
• Anticoagulants are used to eliminate blood clots in small vessels.
• If blood loss exceeds a liter, a donor blood transfusion is necessary.

Treatment of chronic anemia not complicated by serious diseases is carried out on an outpatient basis. Nutrition correction with the addition of foods containing iron, vitamins B9, B12 and C is indicated.

In parallel, treatment is carried out for the underlying disease that caused the pathological changes.

Forecast

If, after extensive blood loss, the patient quickly arrives at the hospital and receives the full range of medical procedures, aimed at restoring blood levels and eliminating bleeding, the prognosis is favorable, except in cases where the blood loss is extremely pronounced.

A chronic type of pathology is successfully eliminated by curing the disease that caused it. The prognosis depends on the severity of concomitant diseases and the degree of neglect of anemia. The sooner the cause is identified and treatment is started, the greater the chances of a favorable outcome.

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