Anemia after excessive blood loss
Introduction
Introduction Anemia after acute blood loss is anemia caused by rapid massive bleeding; anemia after chronic blood loss is small cell anemia caused by long-term moderate bleeding. Seen in chronic gastrointestinal diseases (such as peptic ulcer or acne), chronic bleeding in the urinary or gynecological department.
Cause
Cause
Due to limited bone marrow reserves, anemia can be caused by any type of major bleeding. This bleeding may be caused by spontaneous or traumatic rupture or incision of the large blood vessels, erosion of the arteries by pathological damage (eg, peptic ulcers or tumors), or normal hemostatic dysfunction. The consequences are directly dependent on the length of the bleeding and the amount of bleeding. A sudden loss of one-third of the blood volume may be fatal, but if it is slowly bleeding within 24 hours, even if it reaches 2/3 of the blood volume, there may be no such danger. Symptoms are caused by a sudden decrease in blood volume and subsequent dilution of the blood to reduce the oxygen carrying capacity of the blood.
Examine
an examination
Related inspection
Blood routine dynamic electrocardiogram (Holter monitoring)
Immediately during acute bleeding and immediately after hemorrhage, red blood cell count, hemoglobin and hematocrit are increased due to vasoconstriction. However, within a few hours, the tissue fluid enters the blood circulation to dilute the blood, and the red blood cell count and hemoglobin decrease are consistent with the severity of the bleeding. The anemia produced is normal red blood cell. Increased multinucleated granulocyte and platelet counts may occur during the first few hours. There may be signs of regeneration (reticulocyte increase) in the days after hemorrhage, and there may be an increase in mesenteric cells and mild red blood cells on the blood smear; if the amount of bleeding is large and sudden, occasionally young red blood cells and immature white blood cells may appear. .
Diagnosis
Differential diagnosis
Differential diagnosis of anemia after excessive blood loss:
1. Iron deficiency anemia: iron deficiency affects the anemia caused by hemoglobin synthesis, seen in malnutrition, large amount of small-term bleeding and hookworm disease; as long as women are more likely to suffer from iron deficiency anemia, this is because women Blood loss is fixed every month during the physiological period. Therefore, on average, about 20% of women and 50% of pregnant women have anemia. If the anemia is not very serious, you don't have to eat all kinds of supplements. You can change the symptoms of anemia by adjusting your diet. For example, first of all, pay attention to diet, and balance the intake of iron-rich foods such as liver, egg yolk, and cereals. If the iron ingested in the diet is insufficient or the iron deficiency is serious, iron supplements should be added immediately. Vitamin C can help the absorption of iron, but also help to make hemoglobin, so the intake of vitamin C should be sufficient. Second, eat a variety of fresh vegetables. Many vegetables are rich in iron. Such as black fungus, seaweed, hairy vegetables, leeks, black sesame seeds, lotus root powder and so on.
2. Hemorrhagic anemia: caused by acute massive bleeding (such as gastric and duodenal ulcer disease, rupture of esophageal varices or trauma).
3. Hemolytic anemia: anemia caused by excessive destruction of red blood cells, but less common; often accompanied by jaundice, known as "hemolytic jaundice."
4. megaloblastic anemia: anemia caused by lack of red blood cell maturation factors, lack of folate or vitamin B12 caused by megaloblastic anemia, more common in infants and pregnant women with long-term malnutrition; megaloblastic anemia refers to a large number of giant bone marrow An anemia of young cells. In fact, megaloblasts are immature red blood cells in various stages that are abnormal in morphology and function. The formation of this megaloblastic cell is the result of defects in DNA synthesis, and the development and maturation of the nucleus lags behind the cytoplasm of hemoglobin. A variety of tissue cells in the body are affected by defects in DNA synthesis, but hematopoietic tissues are most severe, especially erythroid cells. Both granulocyte and megakaryocytes also have morphological changes and a decrease in the number of mature cells. The megaloblasts include immature red blood cells at different developmental stages of protoplasts, early megaloblasts, medium megaloblasts, and megaloblasts. These megaloblasts are larger than the corresponding normal young red blood cells, and the proportion of the nucleus is slightly higher than normal. After Wright staining, the cytoplasm of the original megaloblastic cells is dark blue, without particles, and there is a lightly colored circle around the nucleus; the nucleus is round and dyed purple, the most prominent feature is that the chromatin is granular and separated from each other. The partition is relatively translucent, and sometimes there are small pieces of chromatin separated from each other around the core to form a so-called "clock face" state; the nucleolus is large and blue. As the cells mature, the chromatin retains its granular structure and is difficult to form deep-stained condensed masses. Sometimes megaloblastic cells are less anemia, and the morphology of megaloblasts is often less typical, called megaloblasts. The vast majority of megaloblastic anemia is caused by folic acid and vitamin B12 deficiency, but there are a few exceptions, such as megaloblastic proliferation caused by antimetabolites, erythroleukemia and red blood disease, and iron granulocyte anemia. Increased yolk cells, hereditary whey and sour urine. Regardless of the cause, the morphology of the juvenile cells is the same. After proper treatment, these giant young cells can quickly become normal immature red blood cells. Giant erythrocyte anemia may be relatively iron-deficient in the later stages of treatment, and attention should be paid to the timely supplementation of iron.
5. Pernicious anemia: megaloblastic anemia lacking internal factors.
6. Aplastic anemia: accompanied by gastric acid deficiency and spinal column, posterior column atrophy, slow course; anemia caused by hematopoietic dysfunction, aplastic anemia (AA, referred to as aplastic anemia), is caused by a variety of causes of bone marrow Stem cells, hematopoietic microenvironment damage and changes in immune mechanisms lead to bone marrow hematopoietic failure, and diseases with a decrease in whole blood cells (erythrocytes, granulocytes, and platelets) are the main manifestations. The pathological changes of aplastic anemia are mainly the fatification of red bone marrow, which means that the red bone marrow with the hematopoietic function is replaced by fat. The greater the number of substitution, the more severe the anemia. According to the onset of illness, severity of illness, degree of bone marrow destruction and outcome, it is divided into acute and chronic types. In some areas of China, there are 1.87 to 2.1 cases per 100,000 people, which is similar to the reported incidence in Japan. All age groups can develop disease, but it is more common in young adults, more men than women. The ratio of acute to chronic cases was 1:4.6. Aplastic anemia seems to belong to the category of "flawlessness", "deficiency" and "blood syndrome" in traditional Chinese medicine. In the past, it was considered to be an incurable disease. After more than 40 years of practice in the treatment of integrated Chinese and Western medicine, its prognosis has changed. According to the survey, the average age of death has increased, the mortality rate has decreased, and the prevalence rate has increased. Patients with aplastic anemia should pay attention to prevent cross-infection and try not to go to public places. The house should be ventilated. Do not take drugs such as doxycycline, chloramphenicol, sulfonamides, antipyretic and painkillers.
