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CHRONIC POST-HEMORRHAGIC ANEMIA

Chronic post-hemorrhagic anemia develops as a result of either a single, but abundant blood loss, or minor, but prolonged repeated blood loss (Fig. 38).

Most often chronic post-hemorrhagic anemia is observed when bleeding from the gastrointestinal tract (ulcer, cancer, hemorrhoids), renal, uterine. Even occult blood loss during ulcerative or neoplastic processes in the gastrointestinal tract or insignificant hemorrhoidal bleeding, repeated day after day, can lead to severe anemia.

Often the source of the bleeding is so minor 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 nutritional iron needed 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 body's “iron fund”, resulting in severe iron deficiency anemia.

Other things being equal, the development of anemia will occur the easier, the less iron is available in the body and the more (in total) blood loss.

Fig. 38

Hematopoiesis and blood destruction in post-hemorrhagic anemia.



Clinic. Complaints of patients are reduced mainly to severe weakness, frequent dizziness and usually correspond to the degree of anemia. Sometimes, however, strikes a discrepancy between the subjective state of the patient and his appearance.

The appearance of the patient is very characteristic: a sharp pallor with a wax-like skin tone, bloodless mucous lips, conjunctiva, puffy face, lower limbs are pastous, and sometimes, due to hydremia and hypoproteinemia, general edema (anasarca) develops. As a rule, patients with anemia are not exhausted, unless exhaustion is caused by the underlying disease (stomach or intestinal cancer). Anemic cardiac noises are noted, the systolic murmur at the apex, carried out on the pulmonary artery is most often heard; on the jugular veins marked "the noise of the top."

A picture of blood. The blood picture is characterized by iron deficiency anemia with a sharp decrease in the color index (0.6–0.4); degenerative changes of erythrocytes prevail over regenerative; hypocytochrome and microcytosis, poikilocytosis and schizocytosis of erythrocytes (Table 18); leukopenia (if there are no special moments contributing to the development of leukocytosis); shift of a neutrophilic row to the left and relative lymphocytosis; platelet count is normal or slightly reduced.

The next phase of the disease is characterized by a decline in the blood-forming activity of the bone marrow — anemia takes on a hyporegenerative nature. At the same time, along with the progressive development of anemia, an increase in the color index is observed, which is approaching unity; anisocytosis and anisochromia are noted in the blood: along with pale microcytes, more intensely stained macrocytes are found.

The serum of patients with chronic post-hemorrhagic anemia is distinguished by a pale coloration due to a reduced bilirubin content (which indicates a reduced blood breakdown).
The peculiarity of chronic post-hemorrhagic anemia is also a sharp decrease in the level of serum iron, often determined only in the form of traces.

Bone marrow blood formation. In acute cases in healthy individuals, a normal physiological response to blood loss is more often observed, with the development of initially immature, polychromatophilic elements, and then mature, completely hemoglobinized erythrocytes. In cases of repeated bleeding, leading to depletion of the "iron fund" of the body, there is a violation of erythropoiesis in the hemoglobinization phase of normoblasts. As a result, some of the cells die, “not having time to flourish,” or enter the peripheral blood in the form of sharply hypochromic poikilocytes and microcytes. Further, as the anemia acquires a chronic course, the initial intensity of erythropoiesis falls and is replaced by a picture of its oppression. Morphologically, this is reflected 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 blood formation are reversible, since we are talking about the hyporegenerative (not hypoplastic) state of the bone marrow (see Hyporegenerative anemias).

Treatment. In cases where this is possible, the best method of treatment is to remove the source of blood loss, for example, excision of hemorrhoids, resection of the stomach in a bleeding ulcer, extirpation of a fibromatous uterus, etc. However, a radical cure of the underlying disease is not always possible (for example, in inoperable gastric cancer) .

For the stimulation of erythropoiesis, as well as as replacement therapy, it is necessary to perform repeated blood transfusions, preferably in the form of red blood cell transfusions. The dosage and frequency of blood transfusions (erythrocyte mass) varies depending on individual conditions; they are mainly determined by the degree of anemization and the effectiveness of therapy. With a moderate degree of anemization, medium-dose transfusions 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 a patient, blood transfusions are made at a higher 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).

Vitamin B12 therapy for post-hemorrhagic anemia with iron deficiency is indicated for hyporegenerative forms occurring with macronormoblastic type of erythropoiesis and macroscopic erythrocytes.
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CHRONIC POST-HEMORRHAGIC ANEMIA

  1. Iron deficiency anemia is secondary due to blood loss (chronic). Acute post-hemorrhagic anemia
    ICD-10 cipher Iron deficiency anemia secondary due to blood loss (chronic) D50.0 Acute post-hemorrhagic anemia D62 Diagnosis When making a diagnosis Mandatory Level of consciousness, frequency and effectiveness of respiration, pulse, blood pressure, history, thorough physical examination, skin, joints condition Laboratory tests Research: hemoglobin, PTV (PTI), APTTV,
  2. Chronic post-hemorrhagic anemia
    It develops as a result of long-lasting non-abundant bleeding. Chronic post-hemorrhagic anemia in children is the main cause of iron deficiency. The following pathological conditions can be the causes of repeated small blood loss: 1. Diseases of the gastrointestinal tract: erosive and ulcerative lesions of the gastrointestinal tract, polyposis, diaphragmatic hernia, mucous membrane duplication
  3. Acute post-hemorrhagic anemia
    This condition develops as a result of a single massive blood loss. The reasons leading to the development of acute post-hemorrhagic anemia in children of different age groups are presented in Table. 12. Clinical picture Small blood loss in older children does not cause marked clinical symptoms and is relatively well tolerated. Significant blood loss to children is tolerated.
  4. Acute Post-Hemorrhagic Anemia
    Causes of acute anemia from blood loss are various external injuries (injuries), accompanied by damage to blood vessels, or bleeding from internal organs. Gastrointestinal bleeding, bleeding into the abdominal cavity (rupture of the fallopian tube in ectopic pregnancy), renal, pulmonary (tuberculosis, abscess), uterine, and also bleeding are most commonly observed.
  5. Anemia Acute post-hemorrhagic anemia (code D 62)
    Definition Clinical symptom complex caused by massive single blood loss, characterized by hypovolemia and normochromic anemia. Etiology, pathogenesis. A one-time loss of more than 500 ml of blood due to internal or external bleeding leads to hypovolemia with the subsequent development of normochromic anemia, stimulation of hemopoiesis and restoration of the initial parameters of peripheral
  6. Chronic hemolytic anemia
    Chronic hemolytic anemia is one of the typical diseases in children. The disease is characterized by shortening the life of red blood cells (the average period of red blood cell circulation in peripheral blood is about 120 days). Therefore, the severity of the disease depends on the actual shortening of the survival period. Most cases are due to hereditary reasons, but there are also acquired variants.
  7. Chronic iron deficiency anemia (codes D 50.0, D 50.8)
    Definition The disease, the leading symptom of which is a decrease in the number of erythrocytes of less than 4.0 x 1012 / l and hemoglobin of less than 120 g / l with a color index below 0.8 and serum iron levels of less than 13 μmol / l. Statistics. One of the most common human diseases. Up to 25% of the total population, 40% of women of child-bearing age, 33% of persons of both sexes over 60 are affected. Etiology.
  8. ACQUIRED AUTOIMMUNE CHRONIC HEMOLYTIC ANEMIA
    Etiology and pathogenesis. In the light of modern immunohematology, most of the acquired chronic hemolytic anemias are considered from the point of view of autoimmunization of the organism. The cause of immunization can be transferred infectious, in particular viral, diseases (influenza, pneumonia), under the influence of which autoantibodies are formed that have specific agglutination properties according to
  9. CHRONIC HEMOLYTIC ANEMIA WITH CONSTANT HEMOSIDERINURIA AND PAROXISMAL NIGHT HEMOGLOBINURIA (PNH). Markiafaw's disease
    The disease is a special form of chronic hemolytic anemia, characterized by intravascular hemolysis. A distinctive feature of the disease is a constant urine hemosiderin, and at times free hemoglobin. The disease occurs mainly in people of middle age (20-40 years). It is characterized by chronic cyclical course with a tendency to exacerbations under
  10. ADDISON'S ILLNESS — BIRMERA (Malignant Malostomy, Perinitaleal Anemia, B12-Deficiency Anemia)
    The disease described by Addison in 1855 and Biermer in 1868 gained fame among doctors as pernicious anemia, i.e., a fatal, malignant disease. Only in 1926, in connection with the discovery of the hepatic therapy of pernicious anemia, the idea that the incomparability of this disease, which had prevailed for a century, was rejected for a century. Clinic. People older than 40 years usually get sick.
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