Blood test in acute posthemorrhagic anemia. Posthemorrhagic anemia is a complication of herb. Signs and course of the chronic form

Posthemorrhagic anemia is a symptom complex that appears due to the presence of bleeding in the human body. Pathology is characterized by a number of specific clinical and diagnostic features by which it can be recognized and treated.

Classification of posthemorrhagic anemia

Experts offer several classifications of posthemorrhagic anemia. In accordance with the type of flow, the following forms are distinguished:

Acute. Symptoms are acute and progress rapidly. This type of anemia usually occurs with severe trauma, internal bleeding, or surgical damage to large arteries.
Chronic. Signs of anemia develop gradually, usually they are less pronounced than in the acute form. Most often, such anemia occurs with peptic ulcer, hemorrhoidal bleeding, menstrual disorders in patients.

In accordance with another classification, the disease is characterized by the level of its severity:

light - above 90 g / l;
medium - 70-90 g / l;
severe - 50-70 g / l;
very heavy - less than 50 g / l.

Separately, a special form of posthemorrhagic anemia is distinguished - congenital anemia in newborns.

Causes of the disease

The direct cause for the occurrence of a post-hemorrhagic form of anemia in a patient can be considered the presence of a hemorrhage, which can be internal (without blood reaching the surface of the skin) or external.

Acute form of the disease appears in the following cases:

violation of the integrity of large arteries and veins (traumatic or surgical wounds);
rupture of the walls of the heart during heart attacks;
pulmonary hemorrhages;
rupture of aneurysms (stretched walls) of blood vessels;
ectopic pregnancy, accompanied by rupture of the fallopian tube;
heavy menstrual bleeding (menorrhagia);
rupture of the spleen as a result of severe trauma;
severe bleeding from a duodenal or stomach ulcer.

In newborn infants, acute anemia may occur due to birth trauma or placental bleeding.

Chronic form of posthemorrhagic anemia occurs when the patient's body loses small amounts of blood, but constantly. The following factors for the development of chronic posthemorrhagic anemia are distinguished:

mild hemorrhages with peptic ulcer;
hemorrhoidal bleeding;
hematuria (loss of blood in the urine due to damage to the kidneys);
persistent nosebleeds;
tumors of the gastrointestinal tract (colon cancer, neoplasms in the stomach);
blood clotting disorders (DIC, hemophilia).

In some cases, posthemorrhagic anemia develops with scurvy, a disease that occurs when there is a lack of vitamin C.

Symptoms of posthemorrhagic anemia

The clinical picture of the disease is generally uniform, but the severity of symptoms depends on the rate and amount of blood loss.

The acute form of the disease is characterized by the following symptoms:

dizziness;
pale skin and visible mucous membranes (mouth, nose);
shortness of breath, rapid breathing;
severe weakness;
lethargy;
the appearance of noise in the ears;
flashing flies before the eyes, a sharp decrease in visual acuity;
dry mouth;
the occurrence of cold sweat;
decrease in skin temperature, especially hands and feet.

With prolonged acute blood loss, normal blood circulation in vital organs is disturbed, therefore, symptoms of their damage are added. Perhaps the development of multiple organ failure.

Far advanced posthemorrhagic anemia leads to the fact that the patient develops hemorrhagic shock. It is characterized by the following symptoms:

thready pulse on the radial artery;
superficial rapid breathing;
repeated vomiting;
convulsions;
a sharp decrease in pressure;
loss of consciousness.

In critical cases, acute cerebral hypoxia may develop, which, in the absence of resuscitation measures, can lead to the death of the patient.

The course of chronic anemia is characterized by less severe symptoms. Patients usually feel unwell, they often feel dizzy, there is tinnitus, flies flicker before their eyes. Blood loss is compensated for by the reserve capacity of the body for a long time, so chronic bleeding does not lead to the development of acute life-threatening conditions.

Diagnosis of the disease

Diagnosis is carried out using the analysis of clinical data, laboratory and instrumental studies. The volume of the diagnostic complex is determined by the doctor individually in each case. It is important not only to determine the presence of anemia, but also to identify the disease that caused it.

Confirmation of the diagnosis of anemia

When contacting a doctor, the patient describes in detail his clinical picture.

It is important to talk about all the symptoms, even the most minor ones, and also describe in detail how they developed over time.

After that, the doctor conducts an examination. He draws attention to the following signs of anemia:

low blood pressure;
rapid shallow breathing;
increased heart rate, violation of its rhythm;
muffled heart sounds;
systolic murmurs heard at the apex of the heart.

This symptom complex allows you to suspect anemia in a patient and prescribe a number of diagnostic procedures:

general blood and urine tests;
biochemical blood test;
ultrasonography;
according to indications - puncture of the bone marrow.

The gold standard in diagnosing posthemorrhagic anemia is the detection of characteristic changes in the general blood test. In the study, a reduced content of red blood cells is determined, as well as a decrease in the level of hemoglobin. According to these indicators, the presence of anemia is confirmed and its severity is determined.

With a slight blood loss or with a chronic form of the disease, changes in the general blood test may not be immediately determined. They can usually be detected only on the 3-4th day, since until this moment pathological disorders are compensated by the reserve capabilities of the blood system.

The detection of acute anemia, especially in severe forms, requires the initiation of therapy immediately after the diagnosis is made.

In severe cases of posthemorrhagic anemia, when it is difficult to establish the cause of its occurrence, a bone marrow puncture may be required. This study helps to assess the activity of hematopoiesis and detect signs characteristic of pathology.

With prolonged posthemorrhagic anemia, characteristic changes also occur in other hematopoietic organs - the liver and spleen. They determine the foci in which the formation of new erythrocytes occurs.

Determination of the factor that caused anemia

The cause of posthemorrhagic anemia is determined by other studies. For example, a large number of red blood cells can be detected in a general urine test, which suggests that a decrease in hemoglobin in the blood is associated with kidney disease.

On the ECG, you can establish violations of the heart. With ultrasound, doctors determine signs of damage to internal organs (liver, spleen). Symptoms of liver failure can be determined using a biochemical analysis, which detects an increase in the level of enzymes and bilirubin, indicating a malfunction of the organ.

If you suspect gastrointestinal bleeding that occurs with duodenal ulcer or stomach ulcer, the patient undergoes an endoscopic examination - FGDS. It makes it possible to detect a defect in the wall of an organ and, if possible, eliminate bleeding with the help of coagulation.

Treatment of posthemorrhagic anemia

Of paramount importance in the treatment of the disease is the immediate identification of the source of bleeding (damaged vessels) and its elimination. Depending on the area in which the damage is localized, this can be used:

suturing or ligation of blood vessels;
electrocoagulation, laser stop bleeding;
the use of local agents for rapid blood clotting (hemostatic sponges);
resection or removal of organs (in severe cases - with extensive bleeding from stomach ulcers or rupture of the spleen).

An obligatory component in posthemorrhagic anemia with an acute course is infusion-transfusion therapy. Depending on the blood loss, the patient is transfused:

crystalloids (Ringer's solution, Trisol, Disol);
colloids (dextrans, albumin);
frozen plasma;
blood components (erythrocyte, platelet mass).

With light blood loss (up to 20% of the volume of circulating blood), crystalloid or colloid solutions are transfused to the patient. Average blood loss (20-30% of the BCC) requires the appointment of frozen plasma and blood components. In severe cases (more than 30% of the BCC), red blood cells or whole blood are used. The volume of transfusion is calculated individually.

During the introduction of solutions, it is necessary to monitor the patient's condition. The doctor must control the level of his blood pressure and pulse, as this makes it possible to assess the rate of normalization of blood circulation.

Treatment of chronic posthemorrhagic anemia does not require emergency measures. With this form, the main goal of treatment is to eliminate the cause of bleeding. The patient is prescribed iron preparations that stimulate the synthesis of hemoglobin in the body.

Forecast

The prognosis for the patient depends on the type of anemia. A patient with a chronic form of the disease, with proper treatment, quickly recovers, his hemoglobin returns to normal.

In the acute form, the degree of blood loss affects the prognosis. The loss of 1/4 of the volume of circulating blood is a serious threat to the life of the patient and requires resuscitation.

In the absence of treatment and the progression of blood loss, hemorrhagic shock develops. This condition leads to the appearance of acute hypoxia in the vital organs. Insufficient blood supply to the brain with oxygen causes paralysis of the respiratory center, which can lead to the death of the patient.

Prevention

The basis for the prevention of the posthemorrhagic form of anemia is the implementation of the recommendations of specialists:

It is necessary to properly compose the diet so that it includes all the necessary micro and macro elements, as well as vitamins and a sufficient amount of protein.
You need to actively engage in sports, walk in the fresh air.
Treat chronic diseases promptly.
Seek medical attention promptly if symptoms of bleeding occur.

Posthemorrhagic anemia - video

See also a video about the types, pathogenesis, diagnosis and treatment of the disease:

Posthemorrhagic anemia is a serious disease that can lead to the development of serious complications. Pathology has a progressive course, which can lead to the death of the patient, therefore, in case of signs of blood loss, it is recommended to go to the doctor and sign up for an examination.

Posthemorrhagic anemia develops as a result of large blood loss. This is the most common type of disease, it is the result of injuries and chronic diseases, which are accompanied by prolonged internal bleeding.

The loss of a large amount of blood needs to be replaced by iron-containing components in the plasma. Otherwise, the situation is fraught with serious complications up to the death of the patient.

The pathological process proceeds against the background of a significant decrease in the amount of circulating blood. However, the hemoglobin concentration may remain normal.

The danger of the disease lies in the fact that it provokes the development of serious complications in the clinical course of surgical, gynecological and hematological pathologies. In addition, the condition of patients with disorders of the cardiovascular system and the gastrointestinal tract worsens significantly.

Processes in posthemorrhagic anemia

A decrease in hemoglobin concentration and the presence of oxygen starvation of tissues are not the only manifestations of anemia of this type. The loss of blood in a volume of more than 500 ml causes the following negative changes:

An insufficient amount of components such as iron, potassium and magnesium in the body, which inevitably leads to a significant decrease in immunity.
A decrease in BCC (volume of circulating blood) is accompanied by spasms and impaired conduction of blood vessels, and then - a failure in the heart rhythm, instability of blood pressure.
Kidney tissue, skin and muscular system lack blood supply.
As a result of hemorrhagic anemia, urine output is reduced.
Insufficient blood supply to the liver causes its dysfunction.
Due to stagnant processes caused by slow blood flow, acidification of the body with toxins (acidosis) occurs, the presence of which is detrimental to the state of the bone marrow.
A severe degree of anemia provokes the depletion of alkaline reserves, which inevitably leads to the inability to compensate for them.

Such pathological processes make it necessary to urgently correct the patient's condition in order to avoid irreversible processes.

Causes

The main factor influencing the development of posthemorrhagic anemia is acute blood loss, which is a consequence of such conditions as:

mechanical injuries, as a result of which large arteries are damaged;
surgical operations that provoked a complication in the form of bleeding;
stomach or duodenal ulcer;
pathological changes in the liver, accompanied by venous bleeding;
diseases of the genitourinary system and kidneys;
tuberculosis in a chronic form;
abundant and prolonged menstruation, improper attachment of the fetus, severe birth process, cancer of the reproductive organs;
haemorrhoids;
oncological diseases of the gastrointestinal tract.

In adults, nosebleeds, dental procedures, and tooth extractions can also be the cause of significant blood loss.

Clinical picture

The manifestation of characteristic symptoms and signs does not depend on the factors that led to the loss of blood. They are related to its amount and duration of bleeding.

Among the most expressive signs it should be noted:

pallor of the skin;
feeling weak, difficulty breathing;
stuffiness in the ears and noise;
dryness of the mucous membranes of the nose and throat;
chills, feeling of chilliness in the extremities;
frequent but weakened pulse;
lowering blood pressure.

Chronic anemia occurs with less pronounced symptoms, which is explained by the partial compensatory ability of the body.

Possible consequences

Among the possible complications of large blood loss, the following pathological conditions are observed:

malnutrition of internal organs and tissues;
dystrophic changes in the liver, heart muscle (myocardium) and other organs;
disorders associated with the activity of the central nervous system;
convulsions, loss of consciousness;
critical drop in blood pressure.

Due to a sharp violation of the blood supply to the body systems and the subsequent critical decrease in blood pressure, hemorrhagic shock and cardiac arrest occur.

The symptoms of posthemorrhagic anemia are especially difficult for infants to tolerate.

Classification

The clinical picture of the pathological condition gives grounds to distinguish two types of posthemorrhagic anemia.

The acute form is characterized by profuse bleeding caused by external trauma or intense internal hemorrhage.

Damage to the arteries during surgery is also accompanied by an anemic syndrome..

In the chronic course of anemia, moderate blood loss is observed. They are the result of a stomach or duodenal ulcer, hemorrhoids, heavy discharge during menstruation, nosebleeds.

Important indicators

The severity of the disease is determined by the presence in the blood of a component such as hemoglobin. Based on this, three categories are distinguished:

Grade 1 is mild. This substance is at least 90-95 g / l.
2 - medium. The hemoglobin level drops to 75 g/l.
Grade 3 - severe. The concentration of Hb in the blood is only 50-55 g/l.

The identification of indicators below the last indicated indicates that there is an extremely severe degree of the patient's condition.

Stages of development of pathology

The pathogenesis of the acute clinical form is characterized by the manifestation of 3 stages of anemia:

The first stage is vascular-reflex. At this stage, the protective mechanisms of the body are activated, accompanied by the opening of the anastomoses. At the same time, blood pressure decreases significantly, shortness of breath appears, the heart rhythm is disturbed, the skin turns pale.
The second stage is hydremia. The composition of the plasma changes, the vessels are filled with fluid coming from the tissues of the cells. The concentration of red blood cells and hemoglobin in the blood is significantly reduced.
The third stage is changes in the bone marrow. Typical violations occur on the 3-5th day. Iron levels are exceptionally low. This situation requires long-term treatment - up to three months.

The chronic form develops over a long period - from several weeks to a year or more. It is rightfully referred to as iron deficiency manifestations of pathology. Symptoms differ significantly from those of acute anemia.

Among the most expressive signs:

dryness and pallor of the skin;
puffiness;
dullness of hair, fragility of nail plates;
active sweating, indicating weakness;
increased heart rate;
boundary temperature (37 °C).

The lack of timely therapeutic measures to eliminate prolonged bleeding leads to the depletion of the compensatory forces of the body, as a result of which the prerequisites for hemorrhagic shock develop.

Diagnostic measures

Diagnosis of hemorrhagic anemia is a complex process. It involves the study of a combination of anamnestic, laboratory and instrumental indicators.

The goals of examining the patient are to determine the nature of the anemia and to detect the tissues or organ that caused the bleeding.

The main diagnostic steps are as follows:

Interview with the patient. Visual inspection.
Clinical blood test. According to laboratory values, as well as the color index of blood, the duration of bleeding and the change in the concentration of its components are determined. For example, within 1 hour, platelets in the blood rapidly increase. In the next 3-4 hours, blood clotting remains the same, but the concentration of red blood cells and hemoglobin decreases. On the fifth day there is a deficiency in the plasma of iron.
Conducting a biochemical analysis reveals the following picture of the blood: in addition to a decrease in the concentration of iron, there is a low level of calcium and copper, an increase in the level of manganese.

In addition to blood tests, in order to determine the location of bleeding, the following is carried out:

examination of faeces for the presence of occult blood and helminthic invasion;
fibrogastroscopy;
colonoscopy;
sigmoidoscopy;

Laboratory indicators and instrumental examination make it possible to specify the localization of the focus and greatly facilitate the identification of the cause of anemia.

Treatment

The therapeutic course in the acute course of the disease provides for the restoration of the required amount of blood and the normalization of all body systems. Treatment is carried out in a hospital.

To this end:

artificial blood products are introduced - Gelatinol, Poliglukin;
with hemorrhagic shock, significant doses of Prednisolone are prescribed;
removal of symptoms of acidosis is carried out using a solution of soda;
Heparin is used to prevent blood clots.

Direct blood transfusion is used in exceptional cases, as this procedure can lead to an immune-based conflict.

Chronic anemia of this type is treated with iron preparations, if there is no exacerbation of the disease that caused blood loss. In some cases, surgery is performed to remove it.

Health food

Prevention

During the recovery period, the body needs the support of immune forces. Therefore, doctors recommend eating foods rich in vitamins and essential trace elements.

Medicinal extracts of lemongrass, aloe and ginseng have a beneficial effect on the recovery processes.

The chronic form of such a serious disease as posthemorrhagic anemia requires the patient's special attention to his health. Signs of exacerbation are a mandatory indication for immediate medical attention.

Forecasts with timely professional assistance are favorable and guarantee a successful outcome.

What can heartburn lead to, except for sleepless nights and a deterioration in well-being? This symptom is often underestimated by people. In the hope that this is just a temporary uncomfortable condition, the person will not go to the doctor for examination and will not begin treatment.

What complications are observed after diseases accompanied by heartburn? What is posthemorrhagic anemia and what causes it? Why does it happen with GERD?

Posthemorrhagic anemia - a consequence of GERD

Those unfortunate enough to avoid this disease know that gastroesophageal reflux disease, or GERD, is due to weakness of the lower esophageal sphincter. The lower round muscle weakens over time for a number of reasons and begins to pass food from the stomach back into the esophagus. The stomach is acidic, while the esophagus is alkaline. Therefore, when gastric contents get here, a person often feels heartburn. If the symptom of heartburn is ignored even in the initial stages, complications cannot be avoided. These include:

Barrett's esophagus;
strictures or narrowing of the esophagus;
ulcers of the esophagus and as a result - posthemorrhagic anemia.

Posthemorrhagic anemia is a decrease in the amount of hemoglobin in the blood due to bleeding that has developed as a complication of GERD. Anemia occurs after the appearance of ulcerative defects in the mucous membrane of the esophagus or the initial part of the stomach.

Causes of posthemorrhagic anemia

Such a complication of GERD as posthemorrhagic anemia occurs in 2–7% of cases of all complications of gastroesophageal reflux disease. First of all, bleeding does not occur, but ulcers appear on the mucous membrane of the esophagus. The delicate mucous membrane is not accustomed to the acidic gastric contents with hydrochloric acid. The constant impact of the latter leads to gradual trophic disturbances. The nutrition and blood supply of the superficial mucosa deteriorates. If a person continues to ignore all the symptoms that accompany GERD, ulcers appear. Over time, if left untreated, they can reach the muscle layer, in which the vessels are affected. Acute and chronic posthemorrhagic anemia occurs due to blood loss from these "bare" blood vessels.

What causes posthemorrhagic anemia?

In almost 15% of cases, perforation (breakthrough) of the esophageal wall into the mediastinal cavity occurs, while the entire contents of the esophagus through the hole formed can seep into the chest. In addition to food and gastric juice, blood from the affected vessels also flows there.

Symptoms of posthemorrhagic anemia

dry mouth

Acute posthemorrhagic anemia occurs due to severe massive bleeding, while there is a sharp decrease in the number of red blood cells and hemoglobin, but not immediately. How is GERD and its complications related to this? If, due to the appearance of ulcers, small vessels are affected, the bleeding will be insignificant, the person will not immediately feel pronounced changes. A large number of ulcerative lesions of the mucous membrane of the esophagus, or when large vessels are involved in the painful process, bleeding can be severe.

Acute posthemorrhagic anemia develops after the loss of a large amount of blood in a short period of time. In some cases, a person himself does not know about the presence of esophageal ulcers and the appearance of such a GERD complication as bleeding.

Symptoms of the disease depend on the amount of blood lost. The following symptoms indicate the presence of posthemorrhagic anemia.

With a large blood loss, a picture of collapse will develop: a sharp pronounced weakness, bleeding, pallor of the skin, a feeling of dryness in the mouth, vomiting is possible, the person is covered with cold sweat.
Posthemorrhagic iron deficiency anemia is characterized by palpitations, severe muscle weakness, dry skin and the appearance of cracks in the arms and legs, brittle nails. At the same time, there are swelling under the eyes, weakness, constant headaches, nausea, appetite decreases, a person complains of a perversion of taste when eating chalk or clay brings pleasure.

In the case of a large blood loss, symptoms appear almost immediately. In chronic anemia, all of the above symptoms will not occur at the same time, but will develop depending on the amount of blood loss and the frequency of bleeding. In this case, the symptoms will be regular, in the blood test, changes in indicators in a person are noted constantly, until the source of bleeding is detected.

Stages and degrees of posthemorrhagic anemia

An accurate diagnosis of the disease is made after a full examination. The general blood test helps in this. Since posthemorrhagic anemia is a decrease in the level of erythrocytes and hemoglobin in a certain volume of blood, these indicators are looked at in the first place during the study.

The stages of posthemorrhagic anemia are as follows.

The degree of chronic posthemorrhagic anemia is determined by the amount of hemoglobin.

With a mild degree, the amount of hemoglobin in the blood ranges from 120 to 90 g / l.
The average degree is set at a hemoglobin content of 90–70 g / l.
A hemoglobin level of less than 70 g/l is severe anemia.

Diagnosis of the disease

There are three main types of anemia diagnosis:

according to clinical signs;
laboratory diagnostics;
instrumental research methods.

Each of them is important, because with their help you can detect the disease, the source of bleeding, and set the stage.

Diagnosis of posthemorrhagic anemia is based on the following examinations.

Determination of the amount of hemoglobin and erythrocytes in the general blood test. Additionally, depending on the stage of anemia, young blood cells and atypical ones can be detected in the analysis.
A person with suspected posthemorrhagic anemia must be sent for FGDS or a functional study of the initial part of the digestive system, which can detect ulcers and the source of bleeding. But in rare cases, bleeding is not visible.
A biochemical study or a blood test with the mandatory determination of transferrin and ferritin, hemosiderin are important indicators of changes in blood composition.
Not the last place in the diagnosis of posthemorrhagic anemia is the examination of a person and his complaints.

Treatment of posthemorrhagic anemia

In acute post-hemorrhagic anemia or with a very low hemoglobin content, treatment should be carried out only in a hospital. If necessary, anti-shock measures are taken, bleeding is stopped, blood transfusion is performed in case of massive blood loss.

Treatment of posthemorrhagic chronic anemia consists of prescribing a long course of:

iron-containing preparations;
vitamins C and group B (some complex medicines contain both iron and vitamins);
prescribe a diet with an optimal iron content in foods, preference is given to meat with vegetables (low-fat varieties of beef and pork, rabbit, pork and beef liver, veal, fish).

In conclusion, we repeat that posthemorrhagic anemia develops due to blood loss. If you start GERD and completely ignore the manifestations of this disease, such a complication is not far off. You can avoid it if you control the course of GERD and see a doctor every year.

Posthemorrhagic anemia is caused by a single factor - blood loss. It occurs more often than others, because it accompanies injuries, chronic diseases, complicated by bleeding. Treatment of this pathology is impossible without compensation for lost formed elements (erythrocytes, all types of leukocytes, platelets), plasma with protein and microelements.

Changes in the body with blood loss

It is customary to measure the severity of anemia by a decrease in the level of hemoglobin and the onset of hypoxia (oxygen deficiency) of tissues.

But the clinical course and symptoms of posthemorrhagic anemia are largely due to a lack of iron, copper, magnesium, potassium, loss of protective functions (decreased immunity), and increased sensitivity to any allergens.

The critical volume of blood loss is 500 ml. This is the maximum amount of vital substances that a healthy body is able to gradually restore without treatment on its own. It is allowed, if necessary, to donate to donors.

Small arteries are the first to react to the reduced volume of circulating blood; they spasm in coordination with the sympathetic division of the autonomic nervous system. This is a reflex reaction aimed at maintaining blood pressure at the proper level. However, peripheral resistance increases significantly. Due to the drop in venous blood flow, the heart begins to contract more often, trying to maintain the required minute volume.

The loss of essential trace elements affects the function of the myocardium, the speed of contractions and strength decreases. On the ECG at this time, signs of hypoxia and impaired conduction can be detected.

Shunts open between small arteries and veins, blood rushes through the anastomoses, bypassing the capillary network. The blood supply to the skin, muscles, and kidney tissue immediately deteriorates. This mechanism allows you to protect the local blood supply to the heart and brain even with a loss of 10% of the circulating blood volume.

Plasma deficiency is restored quite quickly due to interstitial fluid. The main fatal disorders remain at the level of microcirculation. A significant decrease in blood pressure contributes to a slowdown in blood flow in the capillaries, thrombosis and complete closure.

In the severe stage of hemorrhagic changes, microthrombi block arterial glomeruli in the renal tissue, reduce fluid filtration through them, and this sharply reduces urine output. In parallel, blood flow in the liver decreases. Long-term irreversible acute posthemorrhagic anemia can lead to liver failure.

As a result of general hypoxia, incompletely oxidized substances accumulate in the tissues, which act as poisons on brain cells, causing a shift towards acidosis (acidification by toxins). In severe anemia, alkaline reserves decrease, and the state of metabolic acidosis cannot be compensated.

Despite a decrease in the number of platelets, blood clotting is accelerated due to a reflex increase in the concentration of certain factors.

This state lasts for several days. Then the general coagulability is normalized. Thrombohemorrhagic syndrome may occur due to the growth of procoagulant substances.

Pathological changes require urgent correction measures, elimination of the causes that caused them.

Types of posthemorrhagic anemia

Clinical classification distinguishes 2 forms of anemia associated with blood loss:

acute posthemorrhagic anemia - occurs against the background of rapid massive blood loss due to injuries, external and internal bleeding, during surgery in case of injury to large vessels;
chronic - accompanies diseases with frequent moderate bleeding (hemorrhoids, peptic ulcer), typical for girls and women with menstrual irregularities, uterine fibromatosis, rarely accompanies nosebleeds.

According to the severity of clinical manifestations, it is customary to take into account the content of hemoglobin in the blood and distinguish between:

mild if hemoglobin is above 90 g/l;
medium degree at a hemoglobin level of 70 to 90 g / l;
severe - hemoglobin index from 50 to 70 g / l;
extremely severe - the amount of hemoglobin is below 50 g / l.

According to the ICD-10 (International Classification of Diseases), acute posthemorrhagic anemia is classified as "Aplastic and others" with the code D62.

As separate conditions associated with the established cause of blood loss, there are:

congenital anemia in the fetus due to blood loss with code P61.3;
chronic posthemorrhagic anemia as secondary iron deficiency with code D50.0.

Learn more about the causes of acute and chronic blood loss

The most common causes of anemia are:

injuries with damage to large vessels of the arterial type;
unforeseen complication of surgical interventions;
pathology of the obstetric and gynecological profile (uterine bleeding with ovarian dysfunction, uterine tumors, ectopic pregnancy, complications during difficult births);
peptic ulcer of the stomach and duodenum;
cirrhosis of the liver with portal hypertension and bleeding from the veins of the esophagus;
chronic pathology of the lungs (tuberculosis, bronchiectasis);
chronic hemorrhoids.

Bleeding from an ulcer depends on its location, the internal curvature of the stomach is more traumatized by food

Signs of acute posthemorrhagic anemia appear immediately against the background of massive bleeding and after stopping:

the patient has a pale skin color, cyanosis of the lips;
covered with clammy cold sweat;
complains of severe weakness, dizziness;
possible fainting;
worried about nausea, rare vomiting;
dry tongue;
palpitations, extrasystoles;
weak thready pulse;
heart sounds are muffled on auscultation;
blood pressure is reduced;
breathing is shallow, rapid;
body temperature below 36 degrees.

Patients complain about the lack of fresh air, can hardly tolerate the heat

With different types of bleeding, you can find:

loose bloody stools (from a stomach ulcer);
bloody sputum with bright scarlet blood expelled by coughing (from pulmonary arteries);
increasing swelling at the site of injury, fracture (internal hematoma);
discharge from the uterus in women.

Internal bleeding is difficult to diagnose. Doctors are based on the general condition of the patient.

Stages of the course of an acute form of anemia

The clinic of acute posthemorrhagic anemia goes through 3 stages:

Vascular reflex- is determined by the inclusion of compensatory mechanisms of self-defense, the opening of arteriovenous anastomoses. There is a drop in blood pressure, pale skin, tachycardia, shortness of breath.
The stage of hydremia - begins after 3–5 hours. From the intercellular spaces, fluid enters the plasma and "floods" the vascular bed. Lasts 2-3 days. In the blood, the number of red blood cells, hemoglobin decreases.
Stage of bone marrow changes- starts from the 4th - 5th day after the injury. Due to the development and progression of hypoxia. Increased blood erythropoietin, the level of reticulocytes. By nature, new erythrocytes are defined as hypochromic. The leukocyte formula shifts to the left. Decreased plasma iron levels.

It will take at least two months for treatment and full recovery of indicators.

With menopause, uterine bleeding is accompanied by hormonal changes.

Signs and course of the chronic form

Chronic posthemorrhagic anemia develops after several months or years. Since the basis of pathological changes is the loss of iron, this form rightly refers to iron deficiency states. Symptoms do not differ from the manifestations of iron deficiency in the diet:

skin is pale, dry;
edematous face;
altered taste sensations and attitude to smells;
hair is dull, falls out intensely;
brittle, flattened nails;
increased sweating;
complaints of fatigue, headaches, nausea;
frequent dizziness;
heartbeat;
body temperature slightly above 37 degrees.

Diagnostic methods

Diagnostics aims not only to identify the type of anemia, but also to establish the presence of a bleeding organ or tissues in a chronic process. Therefore, detailed blood tests and additional studies are equally important.

What is found in blood tests?

In case of acute blood loss, the patient must be taken to the hospital, where it is possible to assess the degree of danger of blood loss for human life. Changes in the overall analysis may indicate the duration of bleeding:

in the first hour - the number of platelets increases, the level of erythrocytes and hemoglobin is within the normal range;
after 2-3 hours - with preserved thrombocytosis, neutrophilia appears, blood clotting is sufficient, the number of erythrocytes and hemoglobin decreases, anemia is assessed as normochromic;
after 5 days - the number of reticulocytes grows, a low content of iron in plasma is determined.

In chronic bleeding, oval erythrocytes, leukopenia with lymphocytosis are found in a blood smear. Biochemical tests show the loss of not only iron, but also copper, calcium, and the growth of manganese.

Additional information

To search for a bleeding site, it is necessary to carry out:

analysis of feces for occult blood and helminths;
fibrogastroscopy is necessary to exclude gastric bleeding from an ulcer, a decaying tumor;
colonoscopy - examination of the lower intestines;
sigmoidoscopy - for visual confirmation of the integrity of internal hemorrhoids;
women must consult a gynecologist.

Ultrasound and Doppler studies make it possible to specify the cause of blood loss.

Treatment

Treatment of the acute form is carried out in a hospital against the background or immediately after emergency care and bleeding stops.

To replenish the volume of circulating blood, artificial blood substitutes (Polyglukin, Gelatinol) are transfused, in severe cases they begin to be injected in a jet. With an increase in blood pressure to 100/60 mm Hg. Art. continue drip transfusion.

An intravenous catheter allows long-term transfusion of fluids with drugs

If the patient is in shock, large doses of prednisolone are administered.

Tissue acidosis is removed with a soda solution. Despite blood loss, Heparin is prescribed to relieve thrombosis at the capillary level. The patient is connected to humidified oxygen in the breathing tubes.

The issue of replacement transfusion of donor blood or erythrocyte mass is decided individually. If the operational blood loss is less than 1000 ml, then transfusion is considered contraindicated. The procedure can cause complications such as intravascular coagulation syndrome or immune conflict.

Chronic posthemorrhagic anemia can be treated on an outpatient basis in the absence or exacerbation of the underlying disease. If the cause of blood loss is established, then planned surgery may be required.

The patient's diet must include foods high in iron, vitamins C, B 12, and folic acid.

When treating children, it is imperative to provide the necessary nutrition (complementary foods from 6 months of age). If a child plays sports, then the need for iron increases.

Immunity support is essential during the recovery period. People with posthemorrhagic anemia are susceptible to infection by various microorganisms. For this purpose, a complex of vitamins with microelements, long-term use of immunostimulants (aloe extract, ginseng root, magnolia vine) are needed.

Forecast

Rapid delivery to the hospital and the beginning of hemostatic measures contribute to the successful recovery of the patient. With a large blood loss from large arteries, in the absence of assistance, the patient dies.

Chronic posthemorrhagic anemia can be cured only by eliminating the cause. The patient needs to monitor the signs of exacerbation, start prophylactic treatment in a timely manner, and not postpone the possibility of surgery if it is offered by doctors.

The success of treatment of complications after blood loss depends on the timeliness of seeking medical help.

Etiology

Acute posthemorrhagic anemia characterized by a 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 erythrocytes, leading to impaired oxygenation of body tissues.

Pathogenesis

Hypovolemia - accompanied by stimulation of the sympathetic-adrenal system. Redistributive reactions develop at the level of the capillary network, resulting in phenomena of intravascular aggregation of blood cells. Violation of capillary blood flow leads to the development of hypoxia of tissues and organs, the filling of incompletely oxidized and pathological metabolic products and intoxication, venous return decreases, which leads to a decrease in cardiac output. Microcirculation decompensation occurs due to a combination of vascular spasm with erythrocyte aggregation, which creates conditions for the formation of blood clots. From the moment of formation of signs of erythrocyte aggregation, shock becomes irreversible.

Clinic of acute post-hemorrhagic anemia

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

The acute phase after blood loss, the leading clinical manifestations are hemodynamic disorders (decrease in blood pressure, tachycardia, pallor of the skin, impaired coordination, flesh before the development of a state of shock, loss of consciousness)

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

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

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

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

Diagnosis of post-hemorrhagic anemia

Blood test: decrease in HB, the number of erythrocytes, it is normochromic, normocytic, regenerative - reticulocytes more than 1%

Treatment of acute posthemorrhagic anemia:

Treatment of acute post-hemorrhagic anemia begins with stopping bleeding and anti-shock measures. In order to improve capillary blood flow, the BCC in the body should be replenished; affect the physicochemical properties of blood. In case of severe blood loss, saline solutions are transfused, 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 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 the peripheral blood remains above the lower limit of normal. Clinical symptoms at this stage are not very pronounced, they are manifested by a decrease in tolerance to physical activity.

Iron deficiency anemia develops when the concentration of Hb falls 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 absorption of iron (hemorrhoids and rectal fissures, gastritis, gastric ulcer, etc.) Diseases of the genitourinary system, complicated by micro- and macrohematuria (chronic glomerulo - and pyelonephritis, bladder polyposis, etc.) Increased need for iron: pregnancy, lactation, uncontrolled donation, frequent inflammation.

IDA pathogenesis

Iron is a very important microelement 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 needed in the stomach, which converts it into an oxidized form, the latter in the small intestine binds to the apopheretin protein, forming ferretin, which is absorbed into the blood.

Iron that appears during the destruction of erythrocytes 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.

The iron contained in the body can be conditionally 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 the external environment: it is excreted with feces, lost during hair loss, cell destruction.

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

Clinical picture of IDA

Besides ANEMIC SYNDROME for IDA is characteristic and 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 and lethargic, turgor decreases, brittle nails appear, hair loss, the perception of smells and taste changes – addiction to the smells of gasoline, chalk, acetone, etc. Mucosal changes gastrointestinal tract cheilitis, angular stomatitis, tendency to paradanthosis, dysphagia (Plumer-Vinson syndrome), atrophic gastritis. going on atrophy of the mucous membranes of the eyes in the form of dryness of the eyeball, "symptom of blue sclera", changes in the mucous membranes of the upper and lower respiratory tract, develop atrophic rhinitis, pharyngitis, bronchitis. The muscular system is affected there is a delay in growth and physical development, muscle weakness, weakening of the muscular apparatus of sphincters - imperative urge to urinate, nocturnal anuresis, etc.

Diagnosticsiron deficiency anemia

General blood analysis- decrease in HB, the number of erythrocytes, hypochromia, anisocyto-, poikilocytosis, microcytosis.

Blood chemistry

Decreased serum iron content

Increase in total iron-binding capacity of blood serum

Decreased levels of ferritin and transferrin

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

Principles of treatment with iron preparations:

Dietary iron does not correct iron deficiency.

Preference for preparations containing ferrous iron.

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

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

Treatment within 12 months after the normalization of the content of Hb in maintenance doses to replenish iron stores;

Parenteral iron preparations are prescribed only for malabsorption in intestinal pathology, exacerbation of peptic ulcer, intolerance to iron preparations inside, the need for rapid saturation of the body with iron.

Megaloblastic anemias

(due to deficiency of vitamin B12 and folic acid)

B12- (folic)-deficiency anemia is a group of anemias in which there is a violation of the synthesis of DNA and RNA, 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 anemia

Vitamin B12 deficiency can develop due to malabsorption. This is due to a decrease in the secretion of internal factor Castle (patients after gastric resection, 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 intestine (diphyllobothriasis).

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

The reasons for the development of folic acid deficiency anemia are more often associated with the intake of folic acid antagonists (methotrexate, acyclovir, triamterene), chronic alcoholism, malnutrition, diseases of the small intestine.

Pathogenesis

Deficiency of vitamin B12 leads to a lack of coenzyme methylcobolamine, which in turn affects DNA synthesis, hematopoiesis is disturbed, and atrophy of the mucous membranes of the gastrointestinal tract occurs. With this anemia, the activity of the coenzyme deoxyadenosylcobolamine decreases, which leads to a disruption in the metabolism of fatty acids, the accumulation of methylmalonate and propionate, which causes damage to the nervous system and the development of funcular myelosis.

Folic acid deficiency leads to inefficiency of hematopoiesis with a shortened lifespan of not only erythrocytes, but also other nucleated cells (hemolysis and cytolysis of granulocytes, platelets), a decrease in the number of erythrocytes 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

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

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

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

Possible moderate hepatosplenomegaly - liver enlargement and

spleen

DiagnosticsB12 deficiency anemia

Blood test: a decrease in the amount of hemoglobin and erythrocytes, macrocytic, hyperchromic anemia, basophilic puncture of erythrocytes is detected, which is more typical for B12 anemia (Jolly bodies, Cabot rings);

Bone marrow: erythroid hyperplasia with characteristic megaloblastic type of hematopoiesis in the bone marrow ("blue 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. B 12 for parenteral administration

cyanocobalamin, hydroxycobalamin

Course treatment: 400-500 mcg / day. i / m during the first two weeks; then 400-500 mcg in 1-2 days until the red blood counts return to normal.

If there are signs of funicular myelosis - course treatment of 1000 mcg / day. until the disappearance of all neurological symptoms.

Treatmentfolate deficiency anemia

Folic acid is prescribed at a dose of 3-5 mg / day until clinical remission is achieved. Pregnant women are prescribed in a prophylactic dose of 1 mg / day. An indicator of effectiveness is the reticulocyte crisis on the 6-7th day 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 lifespan of erythrocytes, which is due to their increased destruction and accumulation in the blood of erythrocyte decay products - bilirubin and the appearance of hemosiderin in the urine.

Etiology of hemolytic anemia

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

Pathogenesis

The life span of erythrocytes is normally 100-120 days. It is important to say that anemia develops if the compensatory possibilities of erythropoiesis lag behind the rate of destruction of erythrocytes.

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 in the internal organs and lead to hemosiderosis. At the same time, the amount of urobilin in the urine, stercobilin in the feces increases. With hemolytic anemia, a tendency to form stones in the gallbladder often develops due to the increased content of bilirubin in bile.

Clinic

Hemolysis is characterized by the triad : jaundice, splenomegaly, anemia of varying severity. The severity of jaundice depends on the degree of destruction of erythrocytes on the one hand and on the functional ability of the liver to bind bilirubin. jaundice appears on 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 test: decrease in HB, the number of erythrocytes, normochromic anemia, reticulocytosis, the number of leukocytes and platelets does not change, only after a crisis is leukocytosis possible. 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).

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

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

With autoimmune hemolytic anemia, a positive Coombs test is detected, antibodies to erythrocytes are detected.

Bone marrow: hyperplasia of the red bone marrow due to erythrokaryocytes.

Treatment

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

With autoimmune hemolytic anemia pathogenetic therapy is prescribed - corticosteroids, 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 a deficiency of G-6-PDH should be prohibited from taking "oxidative" drugs (sulfonamides, antimalarials, sulfones, analgesics, chemicals, nitrofurans).

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

Severe course of the disease with functional disorders;

If cholecystectomy is necessary, a splenectomy should be performed at the same time.

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

(HYPO)-APLASTIC ANEMIA

Aplastic anemia is characterized by a deep suppression of bone marrow hematopoiesis and pancytopenia, which determines the main manifestations of the disease.

According to the etiological factor, there are:

Acquired forms (exposure to chemical and physical agents, drugs, 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, such syndromes are characteristic as anemic, hemorrhagic, immunocompromised and febrile.

Hemorrhagic syndrome due to the inhibition of the platelet sheet, manifests itself in the form of rashes in the petichian-spotted type, hemorrhages throughout the body, bleeding of the nose, uterine, gastrointestinal and others. The syndrome of immunodeficiency is manifested by inhibition of the activity of leukocytes and a decrease in the body's immune resistance. This is manifested by frequent colds: tonsillitis, bronchitis, pneumonia. The febrile syndrome is characterized by an increase in temperature to subfebrile figures, weakness, chills.

Diagnosis of hypo-aplastic anemia

General blood analysis- anemia normochromic moderate anisocytosis and poikilocytosis, the number of reticulocytes is reduced, leukocytopenia, thrombopenia

Biochemical analysis blood: the concentration of serum iron is increased. Determination of the renal complex, bilirubin and its fractions (hemolytic and anemia associated with dysregulation 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 classical type of acquired aplastic anemia.

Treatment:

Mode: cancellation of all drugs to which there is an individual hypersensitivity.

Medical treatment:

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

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

3. Replacement therapy:

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

transfusion of platelet mass (for hemorrhages).

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

5. Antibiotic therapy for infectious complications.

Surgical treatment: bone marrow transplantation, removal of the organ that produces antibodies - splenectomy