What it is?
When a person in the blood plasma, after an obvious blood loss, is diagnosed with a lack of elements containing iron, then they talk about posthemorrhagic anemia. Its other name, or rather a more general concept, is anemia - a decrease in the amount of hemoglobin in the blood not tied to its loss.
Posthemorrhagic deficiency of iron-containing blood elements can be acute and chronic. If the patient suffers from frequent bleeding, even in a small amount, this is a chronic form of anemia. If the loss of blood occurred suddenly, and in a considerable amount, we are talking about acute anemia. The minimum amount of blood loss for adults that poses a threat to life is 500 ml.
Severity of anemia after blood loss
In total, there are four degrees of blood loss - mild, moderate, severe and massive, consider the two most significant of them.
Light
Treatment of a timely identified disease is not particularly difficult. It is often enough to resort to taking drugs that will make up for the iron deficiency in the body and the patient will get better. As a rule, course therapy is required, which will take at least three months. The patient may be temporarily hospitalized.
heavy
In the event of severe anemia, the victim of the loss of a large volume of blood is immediately placed in a hospital of a medical institution. To bring the patient out of a dangerous state, the following measures are taken:
- stopping bleeding;
- replenishment of blood loss by any means;
- transfusion of an artificial plasma substitute in a volume of at least 500 milliliters;
- measures to raise and stabilize blood pressure.
Kinds
Acute posthemorrhagic anemia
With a large blood loss, as a rule, with damage to the main arteries, or during the operation, when the patient loses about 1/8 of the total blood volume, post-hemorrhagic anemia develops in an acute form, which in turn has several stages.
- In the reflex-vascular stage, arterial mucosal pressure drops sharply, and the skin turns pale, tachycardia occurs. Peripheral vessels spasm due to lack of oxygen, which enters the internal organs. The body, on its own trying to prevent the pressure from dropping to critical values, activates the mechanisms for the withdrawal of plasma from the organs and the compensatory return of blood to the heart.
- The patient can stay in the hydremic compensatory stage for several days. Approximately five hours after blood loss, a base will be created for the entry of interstitial fluid into the blood vessels. Being irritated, the necessary receptors begin to be included in maintaining the volume of fluid that circulates through the vessels. Aldosterone is intensively synthesized, preventing the removal of sodium from the body, which in turn retains water. But at the same time, plasma liquefaction occurs, which leads to a decrease in the level of hemoglobin and red blood cells.
- Acute post-hemorrhagic anemia passes into the bone marrow stage approximately five days after the onset of bleeding. Progression of hypoxia is observed. Erythropoietin levels become higher. The formation of erythrocytes increases, but the hemoglobin values are reduced. This stage is characterized as hypochromic, due to a sharp deficiency in the blood of iron.
Chronic posthemorrhagic anemia
This type of posthemorrhagic anemia, after emergency assistance to the patient to restore the full volume of blood plasma and eliminate iron deficiency, requires treatment of the disease that caused the development of chronic blood loss.
Signs of anemia after bleeding
After blood loss, the development of anemia is manifested by the following symptoms:
- When the loss of blood is large, the victim necessarily has shortness of breath, the heartbeat quickens, a sharp drop in pressure is observed;
- The integuments of the skin / mucous membranes turn pale;
- The patient complains of dizziness. His ears are buzzing, and his eyes are getting dark;
- Not infrequently, vomiting occurs;
- A sudden feeling of dryness in the oral cavity indicates the development of internal bleeding;
- With bleeding in the digestive organs, there is a sharp rise in body temperature, signs of intoxication;
- One of the signs of bleeding inside will be the patient's message about the sensation of squeezing the internal organs;
- The stool becomes black in color.
Cause of posthemorrhagic anemia
Posthemorrhagic anemia can develop due to blood loss in the following cases:
- in case of injury with damage to the artery or other blood vessels;
- with a disease of pulmonary ailmentswhen the patient coughs, blood comes out;
- as a result of the operation;
- with the onset of heavy bleeding in a woman due to an ectopic pregnancy;
- with peptic ulcer in the digestive tract, when internal bleeding develops;
- when hemostasis is impaired.
Diagnosis based on a blood test
First of all, when a bleeding victim is admitted to the hospital, it is necessary to conduct a study of his blood in the form of a detailed analysis, which will help to correctly diagnose the degree of anemia and assess the patient's condition. To do this, determine:
- the number of platelets;
- hemoglobin and erythrocyte levels;
- the presence of neutrophilic leukocytosis;
- determining the growth of the number of reticulocytes;
- plasma iron levels.
Carrying out blood tests is necessary for the entire period of recovery of the patient. Depending on the form of anemia, the duration of rehabilitation is different.
Treatment
After providing urgent assistance, when the bleeding is stopped, the victim needs treatment in the inpatient department of a medical institution.
In order to replenish the patient's blood volume, with a sharp drop in pressure, it is necessary to transfuse a blood substitute (stream injection). When the blood pressure values can be raised to 100 to 60, the transfusion can be switched to drip mode.
If the patient is in a state of shock, it may be necessary to administer humidified oxygen, an intravenous catheter for infusion of blood substitutes, and a number of medications.
In some cases, when the volume of blood loss is more than one liter, donor blood transfusions are required, however, this measure is contraindicated with a smaller amount of blood lost - it is fraught with complications in the form of an immune conflict or the development of an intravascular coagulation syndrome.
Post-hemorrhagic anemia of a chronic type provides for outpatient treatment in cases where there is no exacerbation of the underlying disease or there is none at all. It is not excluded the appointment of surgery after the cause of bleeding is established.
In the treatment of anemia, immunostimulants and complex vitamin preparations cannot be dispensed with in order to support the patient's immune system, which during the recovery period is especially vulnerable to infection by pathogens.
Features of the treatment of posthemorrhagic anemia
In children
In order to reduce chronic blood loss in young patients, prevention of nosebleeds is essential. In girls in adolescence, you need to ensure that the menstrual cycle is properly formed.
In the presence of anemia in infants, it is necessary to check the state of health of his mother. Perhaps the treatment will need to start with her.
Iron preparations have a children's form of release. As a rule, they are dosed, taking into account the body weight of the baby.
Children are generally prescribed medication by mouth. In the form of injections, babies receive treatment in a hospital, when there are any contraindications.
The duration of therapy for children is set according to the severity of anemia:
- mild - two months;
- medium - up to four months;
- in severe cases of the disease, treatment lasts at least five months.
In the elderly
It is very difficult to treat anemia in patients of the older age category, due to:
- the symptoms of anemia are often disguised as various diseases of a chronic nature;
- in many cases, anemia in an elderly patient can be combined with infectious diseases of an acute / chronic nature;
- neoplasms can be detected, the state of which is very neglected;
- a set of causes for the development of anemia;
- risk of drug overdose.
For elderly patients, it is important:
- organize a balanced diet;
- carry out individual dosing of medicines and prescribe optimal minimum doses;
- diagnose and treat inflammatory diseases, tumors.
Prevention
Preventive measures for the occurrence of anemia after blood loss come down to caution and a healthy lifestyle. Necessary:
- monitor your health and treat diseases in a timely manner;
- to refuse from bad habits;
- avoid injury;
- eat fully.
The minimum blood loss that poses a danger to the health of an adult is 500 ml. Symptoms are due to the phenomena of acute vascular insufficiency due to the rapid devastation of the vascular bed, loss of plasma. With massive blood loss due to the loss of red blood cells, when there is no longer compensation due to increased heart rate, hypoxia develops.
The prognosis depends on the cause, the rate of bleeding, the amount of blood loss and the adequacy of therapy. With a loss of BCC of more than 50%, the prognosis is unfavorable.
Causes of acute posthemorrhagic anemia
Possible causes of blood loss causing acute posthemorrhagic anemia:
- trauma;
- surgical intervention;
- diseases of the digestive tract (ulcers, tumors, hemorrhoids, varicose veins of the esophagus);
- violations of hemostasis;
- ectopic pregnancy ;
- menstrual irregularities;
- neoplasms in the uterus;
- lung diseases and others.
Symptoms of acute posthemorrhagic anemia
Vascular disorders: drop in arterial and venous pressure, pallor of the skin and mucous membranes, tachycardia, shortness of breath. The severity of these changes is not related to the degree of blood loss, since collapse often occurs in response to pain from an injury that caused blood loss.
In the first minutes of blood loss, the hemoglobin content may even be relatively high due to a decrease in blood volume. Due to the entry of tissue fluid into the vascular bed, these indicators decrease even when bleeding stops. The hematocrit is usually within normal limits, as both red blood cells and iron are lost at the same time (normochromic anemia). On the 2nd day, the level of reticulocytes increases, reaching a maximum on the 4th-7th day (hyperregenerative anemia).
The severity of the condition is determined not only by the amount of blood lost, but also by the rate of blood loss. The source is of great importance: bleeding from the digestive tract may be accompanied by fever, signs of intoxication, an increase in the level of urea in the blood (with a normal creatinine content); abdominal bleeding, even with a small blood loss, can cause symptoms of organ compression and so on.
Diagnosis of acute posthemorrhagic anemia
Diagnosis of hemorrhagic anemia should be based on information about the acute blood loss that has occurred. With external bleeding, diagnosis is usually not difficult. With internal bleeding and collapse, other causes of the condition should be excluded.
Treatment of acute posthemorrhagic anemia
Treatment begins with stopping bleeding. A rapid decrease in hemoglobin below 80 g / l, hematocrit below 25%, plasma proteins below 50 g / l is considered the basis for transfusion therapy (blood transfusion). It is enough to replenish the loss of red blood cells by one third. The primary task of the doctor is to restore the volume of circulating blood by transfusion of colloidal solutions. If polyglucin and gelatinol are absent, glucose solution can be transfused.
Reopoliglyukin and its analogues should not be used in conditions of possible resumption or ongoing bleeding, since they can exhibit antiplatelet properties - reduce blood clotting. To replace the erythrocytes, the erythrocyte mass is transfused. The indications in this case are the obvious massive blood loss (more than 1 liter), the persistence of pallor of the skin and mucous membranes, shortness of breath and tachycardia, despite the restoration of the volume of circulating blood with the help of plasma substitutes.
Fresh frozen plasma and plasma substitutes are infused in a larger volume than was lost, and erythrocytes in a much smaller volume. Massive transfusions of whole blood or erythrocytes exacerbate shock-induced microstasis and contribute to the development of DIC.
Small blood loss is replenished with albumin, saline solutions. Whole blood is transfused in the absence of red blood cells. If there is no canned blood, then freshly citrated blood (freshly harvested) or direct transfusion is used. Without extreme necessity, it is highly undesirable to carry it out due to the presence of microclots in such blood. With surgical blood loss of less than 1 liter, the erythrocyte mass is usually not transfused.
After the end of the acute period, iron preparations, vitamins of groups B, C, E are prescribed. After the signs of anemia disappear, iron preparations in a half dose are prescribed for another 6 months.
Prepared from:
- Davydkin I. L., Kurtov I. V. et al. Blood diseases in outpatient practice. M.: GEOTAR-Media, 2011, p. 192.
- Ershov V. I. Visual hematology. - M.: GEOTAR-Media, 2008, p. 116.
- Zaiko N. N., Byts Yu. V., Ataman A. V. et al. Pathological physiology. - K .: Logos, 1996.
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
except 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 red blood cells, 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 prednisone. 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 deep inhibition 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 numbers, 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
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.
- light - above 90 g / l;
- medium - 70-90 g / l;
- severe - 50-70 g / l;
- very heavy - less than 50 g / l.
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.
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).
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.
The course of chronic anemia is characterized by less pronounced 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.
- general blood and urine tests;
- biochemical blood test;
- ultrasound procedure;
- according to indications - puncture of the bone marrow.
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 determine 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).
During the introduction of solutions, it is necessary to monitor the patient's condition. The doctor must monitor 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.
Chronic posthemorrhagic anemia develops as a result of either a single, but profuse blood loss, or minor, but prolonged repeated blood loss (Fig. 38).
Most often, chronic posthemorrhagic anemia is observed with bleeding from the gastrointestinal tract (ulcer, cancer, hemorrhoids), renal, uterine. Even occult blood loss in ulcerative or neoplastic processes in the gastrointestinal tract or insignificant hemorrhoidal bleeding, repeated every day, can lead to severe anemia.
Often the source of bleeding is so insignificant that it remains unrecognized. To imagine how small blood loss can contribute to the development of significant anemia, it is enough to cite the following data: the daily amount of alimentary iron necessary to maintain the balance of hemoglobin 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 bowel movements not only deprives the body of its daily need for iron, but over time leads to a significant depletion of the "iron fund" of the body, resulting in severe iron deficiency anemia.
Ceteris paribus, the development of anemia will occur the easier, the less iron stores in the body and the more (in total) blood loss.
Clinic. Complaints of patients are reduced mainly to severe weakness, frequent dizziness and usually correspond to the degree of anemia. Sometimes, however, the discrepancy between the subjective state of the patient and his appearance is striking.
The appearance of the patient is very characteristic: a sharp pallor with a waxy skin tone, bloodless mucous membranes of the lips, conjunctiva, the face is puffy, the lower limbs are pasty, sometimes general edema (anasarca) develops due to hydremia and hypoproteinemia. As a rule, people with anemia are not malnourished, unless the malnutrition is caused by an underlying disease (cancer of the stomach or intestines). Anemic heart murmurs are noted, most often a systolic murmur is heard at the apex, which is carried out to the pulmonary artery; on the jugular veins, "the noise of the top" is noted.
Blood picture. The blood picture is characterized by iron deficiency anemia with a sharp decrease in the color index (0.6-0.4); degenerative changes in erythrocytes prevail over regenerative ones; hypocytochromia and microcytosis, poikilocytosis and schizocytosis of erythrocytes (Table 18); leukopenia (if there are no special moments that contribute to the development of leukocytosis); shift of the neutrophil series to the left and relative lymphocytosis; the platelet count is normal or slightly reduced.
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 noted in the blood: along with pale microcytes, more intensely stained macrocytes are found.
The blood serum of patients with chronic posthemorrhagic anemia is pale in color due to a reduced content of bilirubin (which indicates a reduced blood breakdown). A feature of chronic posthemorrhagic anemia is also a sharp decrease in the level of serum iron, which is often determined only in the form of traces.
Bone marrow hematopoiesis. In acute cases, in previously healthy individuals, a normal physiological reaction to blood loss is more often observed with the production of initially immature, polychromatophilic elements, and then mature, completely hemoglobinized erythrocytes. In cases of repeated bleeding, leading to the depletion of the "iron fund" of the body, there is a violation of erythropoiesis in the phase of hemoglobinization of normoblasts. As a result, some of the cells die, “not having time to bloom,” or enter the peripheral blood in the form of sharply hypochromic poikilocytes and microcytes. In the future, as anemia becomes chronic, the initial intensity of erythropoiesis falls and is replaced by a picture of its oppression. 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 (see Hyporegenerator anemia).
Treatment. In cases where possible, the best treatment is to remove the source of blood loss, such as 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) .
To stimulate erythropoiesis, as well as replacement therapy, it is necessary to produce repeated blood transfusions, preferably in the form of red blood cell transfusions. Dosage and frequency of blood (RBC) transfusions vary according to individual conditions; they are mainly determined by the degree of anemization and the effectiveness of therapy. With a moderate degree of anemization, transfusions of medium doses are recommended: 200-250 ml of whole blood or 125-150 ml of erythrocyte mass with an interval of 5-6 days.
With a sharp anemization of the patient, hemotransfusions are performed in a larger dosage: 400-500 ml of whole blood or 200-250 ml of erythrocyte mass with an interval of 3-4 days.
The appointment of iron is very important. Iron treatment is carried out according to the general rules for the treatment of iron deficiency anemia (see below).
Therapy with vitamin B12 for iron deficiency posthemorrhagic anemia is indicated for hyporegenerative forms that occur with a macronormoblastic type of erythropoiesis and macroplania of erythrocytes.
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