Acute Anemia: Symptoms, Causes, Treatment and Prevention

It is characterized by reducing the number of circulating red blood cells, the amount of hemoglobin, or the volume of concentrated red blood cells.


Anemia is classified as acute or chronic. Acute anemia denotes a steep fall in the red blood cell population due to hemolysis or acute bleeding. Presenting symptoms such as:

  • The person begins by having pictures of sudden and inexplicable fatigue.
  • The complexion changes to very light or pale tones.
  • Breathing becomes especially difficult.
  • You can experience tachycardia stages.

All this symptomatology ends up causing the person to change moods abruptly without apparent explanation.

In the case of acute hemorrhage, acute bleeding is by far the most common etiology in the emergency department.


The common cause of life-threatening acute anemia is a sudden reduction in the oxygen-carrying capacity of the blood. This may occur with or without reducing intravascular volume, depending on the etiology.

In general, it is accepted that a sharp fall of hemoglobin at a level of 7-8 g / dl is symptomatic, while levels of 4-5 g / dL can be tolerated in chronic anemia since the body can gradually replace the loss of hemoglobin—intravascular volume.

Loss of blood:

Blood loss is the most common cause of acute anemia seen in the emergency department (ED). Iron deficiency anemia is due to chronic slow bleeding and nutritional deficits.


Some life-threatening causes include traumatic injury, massive high or low gastrointestinal bleeding, ruptured ectopic pregnancy, aneurysm, and disseminated intravascular coagulation (DIC).


Sickle cell anemia is caused by a point mutation in the DNA of the beta-globin chain. Valine is replaced by glutamine in the sixth position of the amino acid sequence. In response to oxidative stress, hemoglobin polymerizes, causing stool formation and hemolysis.

In mild sickle syndromes, the hemoglobin level is 9-11 g / dL. In more severe variants, the hemoglobin level is typically 6-8 g / dL.

Patients with sickle cell anemia can have life-threatening complications during acute splenic sequestration and aplastic crisis. The anaplastic turmoil is due to the cessation of erythropoiesis caused by the human parvovirus B19.

Although most adults have undergone autoplenectomy from repeated attacks of micro occlusion in the spleen, young children may have hemoglobin levels of 2 g / dl due to the sequestration of red blood cells.

If the patient survives the initial event, a recurrence rate of 40-50% can be expected.

Thalassemias are characterized by a decrease in the production of globin chains (alpha and beta). Patients with thalassemia major (homozygous for beta-thalassemia) develop severe anemia requiring transfusion in the first year of life.

Other forms of thalassemia can cause acute anemia during periods of oxidative stress.

Abnormality of red blood cell enzyme:

The deficiency of glucose-6-phosphate dehydrogenase (G6PD) and pyruvate kinase (PK) are the two most common enzymatic defects that cause hemolytic anemia. G6PD deficiency affects the pentose phosphate pathway, and PK deficiency affects the glycolytic pathway.

The two variants of G6PD deficiencies are African and Mediterranean. The Mediterranean variant has decreased the enzyme activity in almost all circulating red blood cells.

A potentially fatal hemolytic crisis occurs when the cells are exposed to oxidative stress. In the African variant, only a limited part of the CBR population is vulnerable at any given time; therefore, complications that threaten life are rare.

Congenital coagulopathy:

Von Willebrand’s disease is the most common congenital bleeding disorder. The disease is characterized by a deficient or defective Von Willebrand factor (vWF), essential for platelet adhesion. The transmission is by an autosomal dominant pattern.

Hemophilia A (classic hemophilia):

It is caused by factor VIII deficiency.

Severe bleeding is common:

Transmission is autosomal recessive.

Hemophilia B (Christmas sickness):

It is due to a factor IX deficiency. Only men are affected.


Prehospital care:

The initial care of patients includes:

  • Supplemental oxygen
  • Resuscitation with intravenous fluids (IV).
  • Application of direct pressure to any external bleeding.
  • Fracture splint and fast transport.

Although recent prehospital studies suggest that trauma patients should receive minimal resuscitation with fluids, this view remains unproven and controversial.

The military shock treatment suit is occasionally used in the prehospital setting for trauma patients with pelvic and lower limb injuries. It is contraindicated in patients with pulmonary edema or rupture of the diaphragm. It is also contraindicated in pregnant patients.

Principles of therapy:

Therapeutic approaches to treat acute anemia include:

  • Blood and blood products.
  • Immunotherapies
  • Hormonal/nutritional therapies
  • Adjuvant therapies

The objective of therapy in acute anemia are:

  • Restore the hemodynamics of the vascular system.
  • Replace the lost red blood cells.

The doctor can use mineral and vitamin supplements, blood transfusions, vasopressors, histamine (H2) antagonists, and glucocorticosteroids.

Use of blood and blood products:

Correcting acute anemia often requires blood, blood products, or both.

With significant progressive hemorrhage or hemolysis, blood transfusion alone is insufficient, but providing a timely transfusion to restore hemoglobin to safe levels can prevent considerable complications of acute anemia.

However, although red blood cell transfusion is the fastest way to increase the hemoglobin concentration, that benefit must be balanced with the significant complications associated with transfusion.

Multiple studies have reported worse outcomes (e.g., higher mortality and morbidity rates) in transfused patients compared to non-transfused (or less transfused) patients.

Consequently, a conservative approach is indicated. Although the specific threshold is uncertain, restricting transfusion to patients with hemoglobin levels <6-8 g / dL may be associated with better outcomes.

The whole blood contains red blood cells, platelets, and coagulation factors; however, it is rarely used as a treatment option.

Packaged red blood cells (PRBC) are the remaining components of whole blood after the plasma and platelets are removed. One unit of PRBC is the product of 1 total blood unit and has a volume of 250-300 ml. Each unit of PRBCs is expected to raise the hematocrit level by 3 points.

Each unit of platelets contains 50 ml of plasma and has average amounts of fibrinogen and coagulation factors. A specific decrease in factors V and VII is observed compared to whole blood.

Each platelet unit increases the platelet count by approximately 10,000 / μL. The usual dose in adults is 1 U / 10 kg.

The fresh frozen plasma (FFP for its acronym in English) is the medium that suspends red blood cells and platelets and contains all the coagulation factors.

Patients with factor V and XI deficiency and those with coagulopathies due to liver disease are the best candidates for the administration of FFP; most of the other coagulation factors are now available in concentrated forms.

Additional laboratory studies:

Other studies that may be useful for assessing anemia but that may not apply to the acute ED setting include the following:

  • Iron studies.
  • Levels of folate and vitamin B-12.
  • Levels of lead.
  • Hemoglobin electrophoresis.
  • Bleeding time
  • Bone marrow aspiration.
  • Test of Coombs.

The serum iron test measures the amount of iron bound to transferrin. The reference range is 50-150 μg / dL. The serum ferritin level effectively measures total iron levels in the body. In adult males, the story is 50-150 μg / L. In adult females, the group is 15-50 μg / L.

Transferrin iron-binding capacity (TIBC) is a measure of the total binding capacity of transferrin. The average level is 300-360 μg / dL. The percent saturation of transferrin is serum iron / TIBC.

The reference range is 30-50%. Patients with iron deficiency have levels below 20%, while those with iron overload have greater than 50%.

A significant macrocytosis (MCV> 100) suggests the presence of megaloblastic anemia. Most megaloblastic anemias are due to deficiency of cobalamin (vitamin B-12) or folic acid.

Common causes include inadequate intake, inadequate production of intrinsic factors (i.e., cobalamin deficiency), tropical sprue, parasites (e.g., tapeworms), and drugs.

The anemia associated with lead poisoning is usually normocytic and normochromic.

Symptomatic lead poisoning is seen in children when blood levels are 80 μg / dL. Children may present abdominal pain, lethargy, anorexia, pallor (due to anemia), ataxia, speech difficulties, seizures, and coma in some patients.

Consider hemoglobin electrophoresis if the disease appears or if the patient is of Mediterranean or African origin.

Factor deficiency tests are required to diagnose hemophilia.

Bleeding time is a practical test that measures platelet function. Patients with a bleeding time of more than 10 minutes have an increased risk of bleeding.

This test should always be correlated with normally functioning platelet levels, but very low platelet counts can prolong the bleeding time.


Like the whole spectrum of known anemias, the deficit of some nutrients is constant, with iron being the central one and vitamin B12 and folic acid.

Hence, a balanced diet is one of the best ways to prevent the onset of this disease in our body, and strongly recommends consuming iron-rich foods such as fish, cereals, folic acid, omegas, or nuts; usually, all nuts are rich in iron.

Indeed, to prevent acute anemia, the person has to force himself to have a healthy diet with the same amount of exercise. You should always see your GP when most of the symptoms occur.