What Is Acute Anemia?

various trauma and bleeding during surgery;

artery artery

Acute hemorrhagic anemia

Acute hemorrhagic anemia is caused by trauma or disease caused by rupture of blood vessels, or coagulation, hemostasis, etc., causing a large amount of blood to be lost in a short period of time, which not only affects blood volume but also causes anemia after acute hemorrhage. Iron storage does not decrease in the early stage of its occurrence.

Causes of Acute Hemorrhagic Anemia

various trauma and bleeding during surgery;
artery
major gastrointestinal bleeding caused by diseases such as esophageal or gastric vein rupture, gastric or duodenal ulcer;
ectopic pregnancy, placenta previa, or various obstetrics and gynecological bleeding during delivery;
bleeding in the internal organs, especially the spleen and liver;
massive hemoptysis of lung or bronchi;
Sudden massive bleeding caused by inflammation, tumors, etc. eroding the blood vessel wall;
Various diseases with defective hemostatic mechanisms, especially hemophilia, vascular hemophilia, and bleeding during platelet dysfunction.

Acute hemorrhagic anemia disease pathology

The main pathophysiology of acute massive blood loss is a sudden decrease in blood volume and a decrease in arterial blood pressure. The early compensatory mechanism is to adjust the cardiovascular dynamics and adrenergic stimulation to accelerate the heart rate, increase the cardiac blood transfusion, redistribute the circulating blood volume, and constrict the skin, muscle and spleen, kidney and gastrointestinal tract blood vessels to ensure Blood supply to important organ tissues and organs sensitive to hypoxia such as heart, lung, liver, and brain tissue. The main clinical manifestation during this period was hypovolemia. Because the red blood cells and plasma are lost proportionally, the determination of the hemoglobin and red blood cell volume can still be in the normal range. The recovery of blood volume after 2-3 days mainly depends on the mobilization of water, electrolytes and albumin from outside the blood vessels to expand the plasma volume, dilute the blood, reduce the viscosity, accelerate the blood flow, and help the tissue to take in more oxygen. However, on the other hand, hemoglobin concentration and erythrocyte specific volume continued to decline, leading to anemia. Acute blood loss causes tissue hypoxia, which can stimulate the kidney to produce erythropoietin and promote the proliferation of bone marrow erythropoiesis. After 5 days of acute blood loss, the erythropoiesis reaches its peak. The compensatory capacity of the bone marrow depends on the bone marrow hematopoietic function, the response of erythropoietin, and iron. Whether the supply is plentiful.

Clinical manifestations of acute hemorrhagic anemia

Compensation after blood loss takes a certain amount of time, so the clinical manifestations, in addition to individual status, depend on the amount and speed of blood loss, the presence or absence of complications, and the patient's psychological condition, posture, age, nutritional status, and cardiovascular function. In most young healthy people, the blood loss is below 500 ml, especially the gradual blood loss over several hours, which rarely causes symptoms and does not cause anemia afterwards. About 5% of patients, especially when nervous, fearful, or suddenly sitting up, may have a vasovagal reaction that manifests as weakness, sweating, nausea, slow heart rate, and decreased blood pressure; subsequently, dizziness and even brief syncope. If the blood loss reaches 1000 ml (about 20% of the total blood volume), it may be asymptomatic at rest, but mild cardiovascular symptoms may occur during a short period of activity.
When the bleeding volume increased to 1500-2000 ml (about 40% of the total blood volume), even if the patient was healthy before the bleeding, and bed rest after the bleeding, there was still inevitably thirst, nausea, shortness of breath, extreme dizziness, and even a brief loss of will. Due to the redistribution of blood circulation, the patient's hands and feet were cold, pale, and urine output decreased. The blood pressure, cardiac output, and central venous pressure were all reduced, and the pulse was fast and weak. The patient complained of headaches and gradually developed symptoms of shock, such as irritability, dyspnea, pulse count, skin coldness, nausea and vomiting, and finally coma. If effective rescue measures are not taken, due to obvious hypoxia, tubular necrosis and myocardial infarction can lead to death.
Large and rapid bleeding (about 2500 ml, about 50% of total blood volume), due to the sudden decrease in circulating blood volume, the compensatory function could not fully function, and severe shock soon occurred, leading to death. Patients with pre-existing chronic diseases, infections, malnutrition, dehydration, or pre-existing anemia, even if the blood loss is less than the above amount, can lead to shock or death.

Diagnosis of Acute Hemorrhagic Anemia

Diagnostic criteria for acute hemorrhagic anemia

There is no uniform standard for the diagnosis of anemia after acute blood loss. The clinical diagnosis mainly depends on the history of acute blood loss and the evidence of anemia that occurred within a certain time after blood loss. The following points are recommended for diagnosis.
Have a clear history of acute blood loss and clinical manifestations.
Anemia occurs shortly after acute blood loss.
(3) Reaching the diagnostic criteria for anemia.
If the patient has anemia caused by other reasons, a large amount of blood loss in a short period of time causes a decrease of 20g / L compared with the basic level before the diagnosis of anemia after acute blood loss.
2Anemia does not worsen even after 2-3 days of acute blood loss.
Cardiovascular
Line recovery.

Acute hemorrhagic anemia diagnosis steps

The diagnosis is generally performed according to whether there is recent anemia, recent blood loss, and the site of blood loss.
There are many interfering factors in the diagnosis of anemia after acute blood loss. The development of anemia takes several days and the bone marrow hyperplasia will appear later. Early blood volume decline, blood concentration, blood volume replenishment during the treatment process caused blood dilution, blood transfusion and blood volume replenishment at the same time reduce the severity of anemia. For anemia after acute blood loss, the diagnostic value of haematological examination is limited. Sudden, unexplained anemia requires suspicion of potential bleeding. Evidence of hematopoietic proliferation such as increased reticulocytes and no evidence of excessive destruction of red blood cells is even more highly suspect. The final diagnosis requires finding the bleeding site. Bleeding can be confirmed by analyzing medical history and physical examination imaging examination. Significant anemia caused by a large amount of external bleeding is usually easy to identify. There are also obvious symptoms and signs of major gastrointestinal or female birth canal bleeding. Internal bleeding such as aneurysm rupture may have no obvious external manifestations, but sudden shock, hypotension, and tachycardia should be suspected of the possibility of internal bleeding. Diagnosis of hemorrhage in the retroperitoneum, body cavity, and cysts is difficult. B-ultrasound can help to determine whether there is bleeding and the bleeding site.

Differential diagnosis of acute hemorrhagic anemia

Diagnosis of anemia after acute hemorrhage with a clear history of hemorrhage and evidence of anemia is generally not difficult. but
anemia
Sometimes when the blood loss time, location is not very sure, or there are other factors mixed, it is difficult to judge whether it is anemia after acute blood loss or whether it is only anemia after acute blood loss. Need to pay attention to identify with the following anemia. 1. Acute hemolytic anemia Hematopoietic hyperplasia occurs after acute blood loss, such as increased reticulocytes, which is easily confused with acute hemolytic anemia, but the former has no evidence of red blood cell destruction such as elevated bilirubin. A small amount of acute blood loss is located in the body cavity or interstitial blood loss with red blood cell destruction, and jaundice can also occur, but the degree of red blood cell count and hemoglobin decline is not parallel to the depth of jaundice, and jaundice is generally lighter than hemolysis without hemoglobinuria. This can be distinguished from acute hemolytic anemia.
Anemia with acute infection. Anemia after acute blood loss can sometimes be expressed as moderate fever due to absorption heat generated by bleeding. If it is accompanied by an increase in the total number of white blood cells, it must be identified from acute infection. .

Examination for acute hemorrhagic anemia

Laboratory tests for acute hemorrhagic anemia

Early stage of acute blood loss in peripheral blood
Yellow-green bulbs are seen in the small bile ducts of the liver, which are bilirubin
Only the blood volume decreases sharply, while the hemoglobin and hematocrit can still be within the normal range. The latter cannot be used to estimate the blood loss. After the blood is diluted, the hemoglobin amount and hematocrit will gradually decrease. The most significant anemia at 3 days was normal cells and normal pigmented anemia. Reticulocytes begin to increase within 2 to 3 days after acute blood loss, peaking at 6 to 11 days but generally not exceeding 15% to 30%. Leukocytes also rapidly increased up to (10-20) × 109 / L, up to 35 × 109 / L, mainly due to increased neutrophils, shifted nuclei to the left, and even promyelocytic cells. Platelets began to rise, up to 1000 × 109 / L. Leukocytes and platelets return to normal within 3 to 5 days, and those with persistently elevated leukocyte platelets and reticulocytes must be excluded from potential bleeding.
Bone marrow like bone marrow can be proliferative, mainly young red blood cell proliferation, showing a normal young red blood cell type.
Elevated free bilirubin and serum lactate dehydrogenase increased binding globin decreased and reticulocyte increased.

Other auxiliary tests for acute hemorrhagic anemia

According to clinical manifestations, symptoms and signs, X-ray, CT, MRI, B-ultrasound, ECG biochemistry and other tests were selected.

Treatment of Acute Hemorrhagic Anemia

The principle of treatment should first seek to stop bleeding immediately for the cause of bleeding, on the other hand
Promyelocytic
Take urgent measures to replenish blood volume and prevent shock. Quickly inject normal saline, compound normal saline plasma, dextran human albumin (albumin) or hydroxyethyl starch, and immediately dispense whole blood as soon as possible. After the bleeding stops, further necessary treatment should be performed according to the cause. Anemia itself does not generally require special treatment, and a high-protein, vitamin-rich diet should be given early after the acute phase. If the body's iron storage is sufficient for hematopoiesis, red blood cells will return to normal after 4 to 6 weeks after the bleeding has stopped. Patients with severe anemia at 2 weeks should be transfused with red blood cells to correct anemia. For those with a history of chronic blood loss or previous lack of iron storage, iron can be given after the bleeding has stopped and the condition is stable, to promote the production of red blood cells and the replenishment of iron storage.

Prognosis prevention of acute hemorrhagic anemia

Prognosis of Acute Hemorrhagic Anemia

After active treatment, the prognosis is generally good.

Prevention of Acute Hemorrhagic Anemia

Patients with coagulopathy to avoid trauma should be given early treatment.

Acute hemorrhagic anemia treatment instructions

Acute blood loss may not have an immediate effect on hemoglobin concentration, even if
plasma
The same is true of bleeding that causes severe blood volume that is not enough to cause significant blood vessel collapse. Severe acute bleeding requires immediate blood replenishment, and the replenished blood should be able to recover and maintain sufficient blood perfusion in some important organs. Therefore, the treatment of acute blood loss is mainly based on blood transfusion as soon as possible, so the supplemented blood volume usually does not fully compensate the hemoglobin loss caused by blood loss. Generally, once the dangerous insufficient blood volume has been overcome, the bleeding has also been Stop, the residual anemia must be treated with iron. For moderate anemia, and no further bleeding is possible, when the patient is able to get out of bed without adverse symptoms, and no infection and fever, it is best to give iron treatment instead of multiple blood transfusions.

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