Anemia is a symptomatic complex of a clinical-hematological type that results from a sharp or gradual decrease in the level of hemoglobin with a normal or decreased absolute number of erythrocyte blood cells. This symptom complex unites a whole group of pathological conditions that are similar in clinical and morphological manifestations and differ in the etiopathogenesis of their development.
The human hematopoietic system functions in such a way that in the body the process of both formation and destruction of blood cells of various orders is constantly occurring. In the case of disorders in the blood cell formation system of the erythrocyte series or their increased destruction, conditions are created for the development of anemia of various genesis.
Causes of anemia
The formation of anemia can be triggered by either one or a group of etiological factors, according to which it is customary to distinguish such etiopathogenetic forms of anemia as, for example, alimentary-dependent, posthemorrhagic (provoked by acute or chronic blood loss) and megaloblastic (due to oppression of hematopoiesis processes).
Before considering the pathogenetic mechanisms of the development of anemia, it is necessary to study the modern scheme of hematopoiesis and blood destruction, which occurs in a healthy person under normal conditions. So, according to the modern differentiation of blood cells, which are produced by the bone marrow and undergo different stages of maturation, it is common to distinguish seven types of cellular substrate. The first type is represented by stem cells of myelopoiesis and lymphopoiesis. The second type is the blood precursor cells, from which granulocyte-megakaryocyte-erythrocyte-macrophagal direction and predecessor B- and T-lymphocytes are subsequently formed. The third type is represented by more differentiated classes of blood cells, differing in the degree and rate of hemoglobinization. Maturation and differentiation of these three classes of blood cells is accomplished by mechanisms of humoral regulation, in particular, by erythropoietin. The fourth, fifth and sixth classes are represented by actively dividing and maturing polychromatophilic normocytes, and the seventh type is a mature erythrocyte.
Any chronic or acute anemia is secondary, that is, it is a consequence of an existing pathology in the body (intoxication, tumor damage, vitamin deficiency, endocrine, gastroenterological, gynecological and other diseases).
In the role of the main etiopathogenetic manifestations of anemia, there may be blood loss, inadequate maintenance of substances necessary for blood formation in the human body, toxic effects on the bone marrow, impaired humoral regulation of erythropoiesis, which is observed in hypothyroidism, hypoadrenalism, hypopituitarism, hypogonadism, , increased activity of destruction processes of erythrocyte blood cells.
Symptoms and signs of anemia
Erythrocyte blood cells are the main "transporters" of gases, namely oxygen and carbon dioxide due to the presence of hemoglobin in their composition. In this regard, even a minimal deficit of blood cells of the erythrocyte type, and therefore hemoglobin, provokes the development of hypoxic damage to the structures of the human body, sensitive to oxygen deficiency, as well as the excessive accumulation of under-oxidized substances that disrupt the normal vital activity of organs. The degree of severity of clinical manifestations associated with hypoxia in anemia directly depends on the magnitude and rate of decrease in red blood, as well as the compensatory abilities of the organism.
First of all, anemia affects the structures of the central nervous system, namely the cortex of the brain. Manifestations of anemia regarding the effect on the brain are a diffuse low-intensity headache , a decrease in cognitive abilities, constant drowsiness and at the same time a violation of deep night sleep, a disruption in coordination abilities and a constant sense of tinnitus.
Anemia of severe degree of any etiopathogenetic form is manifested by severe neurologic symptoms and, first of all, by the development of a disturbance of consciousness of varying degrees of intensity (from syncope to anemic coma).
With regard to the hypoxic effect of anemia on the myocardium, a progressive development of dystrophic changes is observed, manifested as a sensation of cardiac disruptions, progressive dyspnea, a tendency to lower blood pressure, nonspecific pain syndrome in the projection of the location of the heart.
Chronic anemia with progressive course is accompanied by the development of cardiosclerosis , which provokes disturbances from the contractile capabilities of the myocardium, which causes the formation of a typical clinical symptom complex of circulatory failure in the severe stage.
In an objective examination of a patient suffering from anemia, attention is drawn not only to the blanching of the skin, but also to a change in the auscultation of the heart. Thus, a decrease in hematocrit and a decrease in the viscosity of the blood is accompanied by an acceleration of the progress of blood through vessels that are reflected in the auscultation of systolic noise at all points of the heart's listening. Above the surface of the cervical veins, as well as in the projection of the femoral triangle, it is often possible to listen to the so-called "whirligig noise".
Hypoxic damage in anemia affects all organs and tissues of the human body, not excluding muscle tissue, so patients suffering from this pathology often complain about the progression of muscle weakness, which has no connection with physical activity. Excess accumulation of under-oxidized substances in the body triggers inflammatory processes, in connection with which, in a patient with a prolonged course of anemia, chronic fever of a subfebrile type can be observed.
When assessing a clinical symptom complex, observed in the patient, it should be taken into account that the various etiopathogenetic forms of anemia can be accompanied by the development of specific clinical manifestations, characteristic exclusively for this pathology.
Degrees of severity of anemia
If we consider anemia from the point of view of the influence on the patient's health, then it is necessary to assess in a comprehensive manner not only the laboratory, but also the clinical indicators available to the patient. Determination of severity of anemia, according to revealed violations of the blood test and data from other instrumental types of research, with any etiopathogenetic form of the disease enters the screening algorithm of the patient's examination and is used to determine the further tactics of treatment.
To differentiate anemia according to the severity, hematologists use a classification, the main criteria of which are the existing clinical symptoms, according to which five degrees of severity are distinguished: the latent stage (completely absent clinical manifestations and the diagnosis is established solely on the basis of laboratory data), moderately expressed stage (reliable anemic and sideropenic symptom complex), a pronounced stage of anemia (reliable clinical manifestations of hypoxic organ damage and disruption hemodynamics of the central type), precoma and coma.
When assessing the laboratory parameters characteristic of anemia, it should be borne in mind that for the establishment of severity is not enough of any one criterion, but only a set of pathognomonic signs of anemia allows you to assess the patient's condition.
For example, at 1 degree of iron deficiency anemia, a decrease in hemosiderin concentration in macrophage cells of the bone marrow is noted, as well as a decrease in the absorption of iron in the small intestine. For the 2nd degree of anemia, an increase in the concentration of protoporphyrin in erythrocyte cells is characteristic, a decrease in the ferritin index, a decrease in the index of sideroblasts, a decrease in the saturation of erythrocytes by hemoglobin, and changes in the morphology of erythrocyte cells according to the type of hypochromia and macrocytosis. For grade 3, not only the progressive deterioration of laboratory parameters is characteristic, but also the development of pathognomonic clinical symptoms of anemia.
Types of anemia
Hematologists in their practice use the division of anemia according to the etiopathogenetic trait, according to which anemia due to deficiency of any factor participating in hematopoiesis, myelotoxic forms of anemia, and anemia caused by increased activity of the destruction process of erythrocyte blood cells are allocated.
Acute hemorrhagic anemia is more often provoked by loss of blood in a volume of at least 500 ml and develops with various traumatic effects on vessels of large and small caliber, which occurs in wounds, surgical interventions and chronic pathologies of internal organs, accompanied by damaging effects on the vessel wall. Clinical manifestations of hemorrhagic anemia consist not only of symptoms of anemia, but also of hemodynamic disorders caused by a rapid decrease in the volume of circulating blood. The pathognomonic sign of acute posthemorrhagic anemia is the worsening of the patient's condition when performing an orthostatic test. Severe anemia is characterized by the rapid development of renal failure. Diagnosis of anemia with existing external signs of hemorrhage, as a rule, does not cause difficulties, and with internal bleeding is based on the indicators of instrumental examination techniques.
The most common etiopathogenetic form of anemia is iron deficiency, which occurs with various pathological conditions (blood loss, impaired absorption of iron in the small intestine, increased iron consumption, fixation by macrophages of iron). The process of absorption of iron, extremely adversely affect the various pathological changes in the mucous membrane of the gastrointestinal tract, observed in diseases of inflammatory, atrophic nature. Iron deficiency anemia in pregnancy develops for other reasons, namely as a result of increased consumption of iron and the processes of redistribution of endogenous iron. Similar etiopathogenesis of anemia development is also observed when a person has any chronic foci of infection ( tuberculosis , syphilis ) and with connective tissue diseases. Alimentary iron deficiency anemia in the baby develops when the rules of natural feeding are not respected, and when the child is transferred to an artificial type of feeding.
Iron deficiency anemia refers to those forms of diseases, the severity of clinical manifestations of which directly depends on the degree of anemia of the organism. All manifestations available to a patient suffering from iron deficiency anemia can be attributed either to the so-called "anemic" or "sideropenic" symptom complex. In addition, the patient may have symptoms that are not related to anemia, caused by manifestations of the main background pathology. With respect to the clinical signs of iron deficiency anemia, it should be borne in mind that most of them do not have high specificity and are observed in other forms of this pathology. When a severe sideropenia is attached to the patient, in addition to non-specific signs of anemia, trophic disorders of the skin and appendages occur in the form of excessive dryness, flaking, fragility of the nail plates, hair loss, and the appearance of seizures. A characteristic sign of anemia is a sharp decrease in appetite until its complete absence, as well as a perversion of taste preferences.
Depending on the characteristics of the course of anemia iron deficiency, several classic options are divided. So, in adolescence, early chlorosis most often debuts, the emergence of which is due to the combination of causes in the form of insufficient intake of iron with food, an increase in iron consumption during the period of intensive growth and puberty, increased by the synthesis of myoglobin and heavy menstrual bleeding. The most common variant of anemia of iron-deficiency anemia is chronic posthemorrhagic, which is observed more among the female half of the population and is caused by frequent and abundant uterine and gastric bleeding. Also at risk for the development of iron deficiency anemia include pregnant women, and the pathogenesis of its development is largely due to increased consumption of endogenous iron.
Megaloblast type of anemia is pathogenetically caused by insufficiency in the body of vitamin B12, resulting in a violation of the synthesis of RNA and DNA by bone marrow cells and switching to a megaloblastic type of hematopoiesis. All megaloblastic forms of anemia, in turn, are divided according to the etiopathogenetic principle into additional variants. The risk group for the development of megaloblastic forms of anemia is made up of persons of elderly age who have a history of stomach or bowel disease of an atrophic nature. A feature of the clinical symptoms of megaloblastic anemia, which distinguishes it from other etiopathogenetic forms of this pathology, is the presence of signs of damage to the structures of the central nervous system. The initial manifestations of the neurological nature is progressive weakness, after which there is a violation of peripheral skin sensitivity, coordination disorders. In some situations, megaloblastic anemia is accompanied by the development of hepatosplenomegaly and toxic damage to the myocardium of the heart. Severe forms of megaloblastic anemia are characterized by more pronounced neurologic symptoms in the form of a disorder of consciousness, neurohumoral regulation of the functioning of internal organs and psychoemotional disorders.
Hemolytic forms of anemia differ in the mechanism of origin, but for all of them a common pathogenesis of development and clinical symptoms are characteristic. Hemolytic anemia often occurs when there are changes in the erythrocyte blood cells themselves, or as a result of external toxic factors affecting erythrocytes (exoerythrocytic hemolytic anemia). Hereditary hemolytic anemia develops as a result of the endogenous pathology of erythrocyte blood cells, while for the acquired forms of this pathology an exoerythrocytic mechanism of development is characteristic.
The classical variant of the course of hemolytic anemia implies the development of anemia, jaundice and splenomegaly in the patient. In some situations, hemolytic anemia can be asymptomatic, but in most cases the patient develops a vivid clinical symptomatology of a crisis character. Manifestations of jaundice is a diffuse change in the coloration of the skin of varying severity. With prolonged course of hemolytic anemia, the patient is palpated with a sharply enlarged spleen and liver, as well as concrements in the bile duct and gall bladder.
Hypoplastic anemia refers to the most unfavorable for prognosis for life and recovery of the patient with a form with a high mortality rate in the young age category, exceeding the 75%. Hypoplastic form of anemia can develop both as a hereditarily deterministic disease, and under the influence of external etiological factors in the form of ionizing radiation, toxic effects of chemicals, infection of the body. Pathogenetic mechanisms of bone marrow hypoplasia development with oppression of red blood of hematopoiesis have not been sufficiently studied to date, which makes it impossible to carry out etiopathogenetic treatment and use of primary prevention of this pathology of blood.
In terms of clinical manifestations of hypoplastic anemia, it should be noted that with this pathology there is a variety of symptoms, each of which can be attributed to one of the three main syndromes: anemic, hemorrhagic and septic-necrotic. In some cases, the patient has an acute debut of hypoplastic anemia in the form of a lightening increase in clinical symptoms and a tendency to rapidly form complications leading to death. However, in most situations, hypoplastic anemia is latent and chronic.
Most often in the role of the first manifestations of hypoplastic anemia are single or multiple subcutaneous hemorrhage in the form of a petechial-spotted rash, as well as not abundant nasal and uterine bleeding. In a situation where neutropenia is attached to the classical course of anemia, the patient has signs of purulent-septic damage to the body, manifested by frequent ulcerative necrotic tonsillitis, panaritium and subcutaneous abscesses, pneumonia. With rapidly increasing septicemia, the patient develops a hectic type of fever, jaundice of the skin and multiple skin hemorrhages.
Diagnosis of anemia
A reliable diagnosis of "anemia" is established not so much on the basis of clinical and instrumental data, but rather taking into account the laboratory criteria of this pathology. Laboratory indicators of anemia are very diverse and their specificity depends on the etiopathogenetic form of the pathology, but there are a number of criteria that are characteristic for all patients suffering from anemia.
Thus, the color index is a kind of marker of saturation of erythrocyte cells with hemoglobin and is determined by the calculation method using a special formula. A clear correlation between the level of the color index and the diameter of red blood cells is noted (with hyperchromic anemia, increased sizes of erythrocytes are observed, and in hypochromic cases, reduced sizes).
A more reliable indicator of the degree of saturation of erythrocyte cells with oxygen is the analysis of the determination of the mean volume of erythrocyte and the mean concentration of hemoglobin in the erythrocyte by the method of blood testing in a special apparatus - a haematolyzer.
A very important laboratory criterion for anemia, reflecting the compensatory capacity of the body, is the determination of the percentage of reticulocytes per unit of blood. Evaluation of reticulocytosis is extremely important as the main marker of the effectiveness of treatment for anemia.
Laboratory tests for anemia caused by iron deficiency are represented not only by a routine study of the blood composition, but also by the determination of the parameters of iron metabolism. Thus, the classical variant of the course of iron deficiency anemia is characterized by the presence of a lowered serum iron level (up to 12 μmol / l), a lower saturation level of transferrin with iron (more than 25%), a positive desferase test, an increase in the iron binding capacity of serum more than 70 μmol / l. In addition to establishing the presence of iron deficiency anemia, it is extremely important to establish the cause of the development of this condition, for which the methods of screening the patient should be used.
For megaloblastic anemia is characterized by the appearance of changes not only in the composition of blood, but also in the bone marrow in the form of hyperplasia of the red germ of hematopoiesis, the presence of a large number of erythroblasts. In addition to the characteristic laboratory manifestations (high color index, poikilocytosis, increase in the size of erythrocyte cells), signs of moderate leukopenia with an unchanged leukocyte formula and giant neutrophils are observed. With regard to other instrumental methods for diagnosis of anemia of the megaloblastic type, the methods of studying the digestive tract are the first place, since it is the pathology of these organs that is the most frequent cause of anemia.
With regard to the diagnosis of hemolytic anemia, the primary criterion is not a reduction in the absolute number of erythrocytes, but a change in their morphology. So, with Minkowski-Schoffar anemia, the prevalence of microspherocytes is prevalent, thalassemia is characterized by the appearance of target red blood cells, and the main criterion for diagnosing sickle cell anemia is the detection of a sickle-shaped erythrocyte in the blood smear. In the hemolytic crisis, in addition to manifestations characteristic of anemia, leukocytosis is observed with a shift of the leukocyte formula to the left and a sharp increase in ESR.
Diagnosis of hypoplastic anemia most often does not cause difficulties, since in this form there is a development of deep pancytopenia in the blood, and the study of sternal punctate allows to establish a decrease in myelocaryocytes and neutrophils against the background of relative lymphocytosis.
Treatment of anemia
The determination of the appropriateness and scope of the necessary therapeutic measures is made solely on the basis of elucidation of the etiopathogenesis of the development of anemia. Thus, in acute posthemorrhagic anemia, the initial treatment consists of immediate stopping of bleeding, normalization of hemodynamic parameters, improvement of blood rheology, replacement therapy with the use of erythrocyte mass in accordance with the severity of anemia.
The applied therapeutic measures for anemia of iron deficiency should be aimed at leveling the root cause of anemia, as well as the elimination of iron deficiency using the pathogenetic drug therapy with iron-containing drugs. When appointing drugs containing iron (Tardiferone 1 tablet twice a day, Ferrum-lem 2 mg intramuscularly once a day), it should be borne in mind that the tolerance of this group of drugs is extremely individual, due to the irritating effect of iron salts on the mucous membrane of the organs of the gastrointestinal tract. The dose of the drug should be selected very carefully, given that the patient may have a limited absorption of iron. To eliminate the limited absorption, hematologists often prescribe a combined use of iron-containing drug and ascorbic acid. With regard to the correction of the patient's eating behavior, it is necessary to enrich the diet with products containing protein.
Parenteral intake of iron-containing agents is carried out only in the case of a patient's disturbed intestinal absorption. The main control indicator, indicating the effectiveness of iron drugs in the treatment of anemia, is an increase in reticulocytosis, a progressive increase in hemoglobin and color index. After the normalization of the blood test for the indices of anemia, the use of prolonged forms of iron preparations is recommended (Aktiferrin 1 capsule per day).
In the megaloblastic type of anemia, the basis of pathogenetic treatment is the purpose of parenteral administration of Cyanocobalamin in a daily dosage of 500 mcg. In general, vitamins for anemia are used in complex drug therapy, as their insufficiency in the body only aggravates the progression of anemia. Cyanocobalamin is characterized by the ability to rapidly accumulate in the structures of the bone marrow and hepatic parenchyma, therefore a positive result from its application in the form of transformation of bone marrow hematopoiesis into normoblastic is observed already during the first two days of therapy. Reticulocyte crisis, as a rule, occurs after a week of regular administration of the drug, and complete normalization of red blood tests is noted on average after one month of pathogenetic treatment. Purpose Folic acid in a daily dosage of 5 mg is advisable only in the case of a proven deficit. After relief of signs of severe anemia, the patient is recommended lifelong intake of Vitamin B12 at a dose of 500 μg twice a month.
Treatment of hemolytic anemia should be selected individually, depending on the pathogenetic form of the syndrome. Thus, with the anemia of Minkowski-Schofar, splenectomy is considered the only effective method of therapy. Indications for surgical treatment include: severe degree of anemia, frequent episodes of hemolysis, frequent attacks of hepatic colic. The proven effectiveness of splenectomy in Minkowski-Schoffar anemia is at least 90% in the form of a sharp decrease in hemolysis, preventing recurrence of anemia. In a situation where the patient, along with hemolytic anemia, has calculous cholecystitis, it is recommended to combine splenectomy and cholecystectomy. The expressed degree of hemolytic anemia should be accompanied by the appointment of transfusion using the erythrocyte mass of one group.
With hereditary hemolytic anemia due to a deficiency of G-6-FDH activity, combined use of detoxification therapy in the form of intravenous injection of 5% glucose solution, transfusion of erythrocyte mass and Riboflavin in a daily dosage of 0.045 mg is shown. In order to prevent the development of DIC-syndrome, it is recommended that subcutaneous administration of Heparin in a single dose of 5000 units be administered four times a day, taking into account the coagulogram indices.
Acquired forms of hemolytic anemia are accompanied by a tendency to develop frequent hemolytic crises, for the relief of which Prednisolone should be applied at a calculated daily dosage of 1 mg per 1 kg of the patient's weight. The criterion for the effectiveness of hormonal therapy is the normalization of body temperature, a reduction in the number of reticulocytes, and a simultaneous increase in red blood. The severe course of acquired hemolytic anemia needs correction using the method of transfusion of erythrocyte mass, and in a situation where the abovementioned methods of treatment do not bring the desired effect, the patient is recommended to perform splenectomy. In addition, the indications for splenectomy with acquired forms of hemolytic anemia include: the autoimmune nature of the disease, the development of complications with the use of glucocorticosteroid drugs. Typically, after splenectomy, there is a lifelong remission, and if this surgical treatment is ineffective, a cytostatic therapy is recommended for the patient.
In paroxysmal nocturnal hemoglobinuria, one of the manifestations of which is hemolytic anemia, transfusion of thawed and washed erythrocytes is the greatest effect in relieving the signs of anemia. The necessary periodicity of performing transfusions is selected strictly individually, taking into account indications and contraindications to the application of the technique (severity of anemia, general condition of the patient, individual reaction of the organism), however, it should be borne in mind that multiple transfusion increases the risk of developing negative posttransfusion reactions. A positive effect on the normalization of red blood indices during paroxysmal nocturnal hemoglobinuria is the combined use of red blood cell transfusions and the intake of anabolic drugs such as Retabolil (intramuscularly in a single dose of 25 mg).
Treatment of patients with signs of hypo - and aplastic anemia should be comprehensive, taking into account the etiopathogenesis of the disease. So, with hypoplastic anemia, provoked by the effect on the bone marrow of myelotoxic factors in the form of medicinal substances and other chemical compounds, the patient's treatment should begin with the elimination of the fact of toxins exposure on the body. The main task pursued by hematologists in the treatment of patients with signs of hypoplastic anemia can be described as "restoration of the function, quantity and normal processes of vital functions of stem cells and elimination of immune reactions negatively affecting the process of hematopoiesis in the bone marrow." Thus, the basis of pathogenetic therapy is the preparation of immunosuppressive action (Antilymphocyte immunoglobulin in a daily dose of 130 mg intravenously drip, Cyclosporin A in a daily calculated dose of 10 mg / kg orally). Despite the positive efficacy of this pharmacological group, there are a number of contraindications to their use in the form of severe hemorrhagic syndrome , infectious and inflammatory complications, severe pathological changes in internal organs. The role of an auxiliary link in the treatment of patients suffering from hypoplastic anemia is transfusion of erythrocyte mass and platelet concentrate. To stimulate the processes of erythropoiesis, the patient is recommended a prolonged use of drugs such as Erythropoietin. In a situation where drug therapy does not bring the desired effect even if it is used for a long time (more than one year), the patient should perform a splenectomy. Extreme measure to eliminate the signs of aplastic anemia is bone marrow transplantation with a thorough immunological selection of the donor bone marrow. When using this technique, it should be borne in mind that its proven effectiveness in hypoplastic anemia is no more than 50%.
Blood transfusion in anemia, as with many other blood diseases, is an important component of complex therapy. Currently, hematologists use not a replacement blood transfusion, but component homotherapy, that is, transfusion of drugs containing only one component of blood, seized by the method of fractionation. For the treatment of patients with anemia, transfusion of thawed and washed erythrocyte cells, as well as erythrocyte mass, is used. The main advantages of red blood cell transfusion are the ability of the erythrocyte mass to provide a coagulating effect by the release of thromboplastin from erythrocytes, as well as the detoxification capacity of red blood cells. Transfusion of erythrocyte mass, in fact, is a safe technique that patients tolerate well, provided that the rules of its application are fully complied with. In some cases, the patient may develop complications after applying transfusion in the form of anaphylactic, pyrogenic and allergic reaction. As a rule, no more than 20 minutes pass from the beginning of the transfusion to the clinical manifestations of complications. To correct posthemotransfusion reactions, preparations of the group of antipyretic agents, desensitizing preparations, and also means normalizing hemodynamic parameters are used. The development of the anaphylactoid reaction belongs to the category of urgent conditions and requires immediate resuscitation (intravenous administration of Prednisolone in a dose of 60 mg, Reopoliglyukin in a volume of 400 ml).
Effects of anemia
The prognosis for complete recovery, as well as the degree of influence of pathological processes occurring in the body in anemia, depends not only on the severity of anemia, but also on the etiopathogenetic form of this pathology. So, iron deficiency anemia, as a rule, is characterized by a favorable course and absence of negative influences on vital organs. Provided that the etiologic factor and prompt pathogenetic treatment are quickly eliminated, complications of iron deficiency anemia are not observed, and the patient fully recovers.
Megaloblastic anemia also belongs to the category of auspicious forms of anemia and the negative consequences in the form of a profound violation of the neurological status of a person develop only if there is a complete lack of medication.
The most severe form of anemia with rapid development of complications is hemolytic, in which the patient is at increased risk of developing intravascular disseminated coagulation syndrome, which, in the absence of timely medication correction, can lead to a lethal outcome of the disease.
With regard to the prognosis for the full recovery of a patient suffering from hemolytic anemia, only the acquired forms of this pathology are considered positive. With hereditary hemolytic anemia due to their lifelong course and the lack of methods of primary prevention, there is a high rate of complications.
The effects of paroxysmal nocturnal hemoglobinuria are extremely unfavorable with respect to the effect on the patient's health in the form of severe anemia, multiple vascular thromboses , progressive renal failure, and thromboembolic complications. In view of the propensity for the rapid development of complications, paroxysmal nocturnal hemoglobinuria is characterized by high rates of mortality.
Hypoplastic anemia belongs to the category of the most unfavorable clinical form, since its course is characterized by the rapid development of hemorrhagic and infectious-toxic complications. In view of the limited application of bone marrow transplantation as the only effective method for treating hypoplastic anemia, the mortality rate of patients achieves critically high values.
Prevention of anemia
Preventive measures in the anemia of any etiopathogenetic form are more concerned with non-drug methods of both primary and secondary prevention. The purpose of primary prevention in anemia is to prevent the development of hematopoietic insufficiency and measures for its use are available only for alimentary-deficient forms of the disease. Preventive measures of secondary nature are used, as a rule, after drug therapy and their action is aimed at preventing recurrence of anemia and the development of complications.
Prevention of iron deficiency anemia is to rationalize the eating behavior of both patients with a history of anemia episodes and absolutely healthy individuals as a primary prevention. Medication prophylaxis of iron deficiency anemia occurs only in pediatrics for children born to mothers with anemia during pregnancy. The preferred dosage form in this case is iron preparations in the form of drops for oral administration. Also in drug prevention women need in the period of breastfeeding and suffering from polymentoria.
Primary prophylaxis in megaloblastic forms of anemia is not performed, and secondary prevention methods consist in regular instrumental examination of the patient for exacerbation of chronic gastroenterological pathologies.
Unfortunately, at present no methods for primary prevention of hereditary hemolytic anemia have been developed, however, in establishing the diagnosis, patients should be restricted to taking any medications of myelotoxic action. Prevention of hypoplastic anemia is similar to that of hemolytic anemia and, unfortunately, does not imply the use of drug prevention of its development.
? Anemia - which doctor will help ? If there is or suspected anemia, immediately consult a specialist such as a hematologist, transfusiologist.