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Acute Anemia

Editor: Ajay Tambe Updated: 8/17/2023 10:48:24 AM


Anemia is a condition characterized by a deficiency in the number of circulating red blood cells (RBCs), the amount of hemoglobin (Hgb), or the volume of packed RBCs (hematocrit).[1] The World Health Organization defines anemia as a hemoglobin level below 13 g/dL in men and below 12 g/dL in women.[2] 

Anemia can be classified into 2 main types: acute and chronic.

  • Acute anemia is a sudden and rapid decrease in RBCs, primarily caused by hemolysis or acute hemorrhage.
  • Chronic anemia is characterized by a gradual decline in RBCs over time. The causes of chronic anemia are diverse and can include conditions such as iron or other nutritional deficiencies, chronic diseases, drug-induced factors, and other underlying causes.


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Anemia can occur as a result of various events and underlying conditions. One of the most prevalent causes of anemia is blood loss, which directly leads to decreased RBCs. Blood loss is particularly common in cases of acute anemia observed in emergency room (ER) settings. Emergent conditions leading to acute anemia include traumatic injury causing arterial bleeding, ruptured aneurysm, massive upper or lower gastrointestinal (GI) hemorrhage, ruptured ectopic pregnancy, and disseminated intravascular coagulation.

Hemolytic anemias can also contribute to acute and chronic anemia, involving the destruction or reduced survival of RBCs. These types of anemias can be classified into 2 main categories: intracorpuscular and extracorpuscular.

Intracorpuscular Hemolytic Anemias: Conditions where the defect or problem lies within the RBC. 

  • Hemoglobinopathies affect the structure or function of Hgb.
    • Sickle cell disease is caused by a point mutation in the DNA of the beta-globin chain, resulting in the production of abnormal Hemoglobin, Hemoglobin S (Hgb S). Under oxidative stress conditions, the Hgb S molecules polymerize and cause the RBCs to assume a sickle shape. These sickled cells are less flexible and can block blood vessels, leading to tissue damage, pain crises, and other complications.
    • Thalassemias are a group of inherited disorders characterized by reduced production of either alpha or beta globin chains of hemoglobin. Alpha thalassemia occurs when there is a deficiency or absence of alpha globin chains, while beta thalassemia occurs due to reduced or absent beta globin chain production. These imbalances in globin chain production result in abnormal hemoglobin synthesis.
  • Enzymopathies involve abnormalities in specific enzymes within RBCs.
    • Glucose-6-phosphate dehydrogenase (G6PD) is an X-linked inherited disorder that affects the pentose phosphate pathway. Hemolysis is often triggered by external factors such as certain medications, infections, or exposure to oxidative stress.
    • Hemophilia A is an X-linked genetic disorder caused by a factor VIII deficiency. Individuals with this condition may experience prolonged bleeding after injuries or surgeries.
    • Pyruvate kinase (PK) deficiency is an autosomal recessive disorder characterized by a deficiency of the PK enzyme. This deficiency leads to a condition known as nonspherocytic anemia.   
    • Phosphofructokinase (PFK) deficiency is an autosomal recessive disorder known as Glycogen Storage Disease or Glycogenesis Type VII. It involves a deficiency of the PFK enzyme. Individuals with PFK deficiency may experience muscle pain, rhabdomyolysis, and hemolytic anemia.
    • Phosphoglycerate kinase (PGK) deficiency is an X-linked metabolic disease characterized by a deficiency of the PGK enzyme. This deficiency leads to various symptoms, including myopathy, splenomegaly, CNS disturbances (eg, seizures and mental retardation), and nonspherocytic hemolytic anemia. 
    • Aldolase deficiency is an autosomal recessive disorder that results in hemolytic anemia due to the deficiency of the aldolase enzyme. Individuals with this deficiency can present with muscle weakness. 
    • Triosephosphate isomerase (TPI) deficiency is an autosomal recessive disease with multisystem effects. This deficiency can lead to various symptoms, including (hemolytic) anemia, intellectual disability, cardiomyopathy, and increased susceptibility to infections. 
    • Membrane-cytoskeletal defects such as hereditary spherocytosis or hereditary elliptocytosis are genetic disorders that affect the constituents of the RBC membrane and cytoskeleton. These defects result in the disfigurement of RBCs, leading to the removal of the spleen.[3][4][5] 
    • Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder characterized by a clonal autoimmune mechanism that leads to hemolysis, thrombosis, and marrow aplasia. 

Extracorpuscular Hemolytic Anemias: Characterized by factors external to the RBC that lead to its destruction.

  • Mechanical destruction (microangiopathic):[6][7][8][9][10]
    • Thrombotic thrombocytopenic purpura (TTP) is a condition in which platelet-rich thrombi form in the small blood vessels. TTP is primarily caused by a deficiency in ADAMTS13, metalloprotease responsible for cleaving von Willebrand factor. A triad characterizes TTP, including microangiopathic hemolytic anemia, severe thrombocytopenia, and organ ischemia.
    • Familial (atypical) hemolytic-uremic syndrome (HUS) is caused by mutations in several genes that encode complement regulatory proteins. These mutations lead to dysregulation of the complement system, resulting in the activation of the immune system and damage to small blood vessels. The characteristic presentation for HUS is the triad, including microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. It is similar to TTP, but lesions are limited to the kidney.
  • Complement-mediated thrombotic microangiopathy: Characterized by abnormal activation of the complement system, leading to the formation of small blood clots in the microvasculature. This can occur in various disorders, including HUS.
  • Immune thrombocytopenic purpura (ITP): A condition in which IgG autoantibodies bind to platelets, marking them for destruction by the spleen. This leads to decreased platelet count, resulting in an increased risk of bleeding when platelet levels become very low.
  • Disseminated intravascular coagulation (DIC): A condition in which widespread systemic activation of coagulation occurs in response to various underlying causes, such as infections, severe trauma, or certain complications during pregnancy. DIC initially leads to excessive formation of intravascular fibrin, causing thrombosis. However, as the coagulation factors are consumed, bleeding complications can arise. 
  • Toxic agents and Drugs: Exposure to substances such as hyperbaric oxygen (or 100% oxygen), certain medications (methyldopa, nitrates, chlorates, methylene blue, dapsone, cisplatin), numerous aromatic (cyclic) compounds, and other chemicals (arsine, stibine, copper, and lead) can result in RBC destruction and hemolysis.
  • Infectious: Malaria is the most common cause of hemolytic anemia worldwide. In some regions, infection with Shiga toxin-producing E.coli O157:H7 causes HUS. In specific clinical scenarios like open wounds, septic abortion, or contaminated blood transfusions, Clostridium perfringens sepsis can induce life-threatening hemolysis through the action of a toxin with lecithinase activity.
  • Autoimmune hemolytic anemia: This condition occurs when IgG antibodies target and bind to RBCs, leading to their destruction by macrophages, resulting in hemolysis. The shape of the affected RBC changes to spherocytes, which are rigid and nonelastic, making them more susceptible to rapid destruction. This anemia can be associated with autoimmune diseases (eg, lupus), certain types of lymphomas, and leukemias, or can be drug-induced. Many times there is no identifiable cause. Hemolysis is caused by immunoglobulin G (IgG) autoantibody binding to the RBCs, resulting in macrophages attacking the RBCs' membrane, changing their shape to spherocytes, which undergo destruction more rapidly due to their rigid, nonelastic shape. 
  • Hypersplenism: This condition refers to splenomegaly that leads to increased destruction of blood cells, including RBCs. In acute etiologies, such as infections or other causes of hemolysis, the spleen removes more red blood cells, intensifying the loss.[11] When hypersplenic destruction outpaces the marrow production of RBCs, the anemia becomes more pronounced.  


Anemia is a common condition, affecting one-fourth of the overall population. The prevalence of anemia is even higher among hospitalized patients, with approximately 50% affected. Among elderly hospitalized patients, the rate of anemia can go up to 75%. 

Data collected in the year 2,000 from over 81,000 health plan members revealed the highest rates of anemia in specific patient populations. Patients with chronic kidney disease had the highest prevalence of anemia, with a rate of 34.5%. Patients with cancer had a prevalence of 21%, while those with chronic heart disease had a rate of 18%. Inflammatory bowel disease accounted for 13% of anemia cases, followed by rheumatoid arthritis at 10%. Additionally, individuals with human immunodeficiency virus (HIV) infection had a prevalence of anemia at  10%.[12]   


Acute anemia can have 2 common causes: hemolysis or hemorrhage, both of which result in a sudden reduction in RBCs.  When the drop in RBCs is rapid, a hemoglobin level of 7 g/dL to 8 g/dL is usually symptomatic because the body has inadequate time to compensate and replace the volume lost. In healthy individuals, a  20% loss of blood volume can be tolerated without significant symptoms due to reflex vasospasm and redistribution of blood flow.

However, as the blood loss increases beyond this threshold, patients begin to exhibit the signs and symptoms of hypovolemia. Compensatory mechanisms, such as redistribution of blood flow, are no longer sufficient to maintain blood pressure, leading to clinical signs such as postural hypotension, altered mental status, cool and clammy skin, tachycardia, and hyperventilation.

In the case of acute hemorrhage, hemoglobin and hematocrit levels can initially be normal because red cells and plasma are lost concomitantly. This becomes apparent after the patient’s plasma volume is restored spontaneously or with intravenous fluids.


When examining a peripheral blood smear under a microscope, specific findings can provide valuable information about the underlying condition. The following are some observations related to certain types of anemia:

  • Microangiopathic Hemolysis (TTP, ITP, HUS, DIC): In conditions characterized by microangiopathic hemolysis, such as thrombotic thrombocytopenic purpura (TTP), immune thrombocytopenic purpura (ITP), hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC), several abnormal RBC shapes may be observed. These include helmet cells (schistocytes), fragmented RBCs, and other RBC fragments. Spherocytes (small, round RBCs lacking central pallor) can also be seen in some cases.
  • Sickle Cell Disease: In sickle cell disease, sickle-shaped cells (also known as sickle cells) are a characteristic finding. These cells have a crescent or "sickle" shape due to the abnormal hemoglobin S (Hgb S) present in individuals with this genetic disorder. Another finding that may be observed in sickle cell disease is Howell-Jolly bodies, which are small nuclear remnants within RBCs. Howell-Jolly bodies are typically seen in individuals with functional asplenia or hyposplenism.

History and Physical


When evaluating a patient with anemia, obtaining a thorough but focused history is essential for guiding further assessment and management. However, specific priorities should be addressed initially, such as managing the patient's airway, breathing, and circulation (ABCs). If necessary, immediate resuscitation measures should be initiated to stabilize the patient.

In cases where the patient cannot communicate, gathering as much information as possible from emergency medical services (EMS) personnel or individuals at the bedside is crucial. Previous medical charts, if available, can also provide valuable insights into the patient's medical history and help in understanding the underlying cause of anemia.

A focused history should also be obtained to identify the potential source of bleeding. For example, if gastrointestinal (GI) hemorrhage is suspected, a more detailed GI history should be obtained, including any previous episodes of GI bleeding, symptoms of gastrointestinal disorders, or known GI conditions. Similarly, if gynecological causes are suspected, a focused menstrual and pregnancy history should be taken to evaluate any potential gynecological sources of bleeding.

Physical Exam

In evaluating a patient with anemia, frequent vital sign monitoring is essential to assess the patient's stability and response to interventions. As mentioned above, the initial physical examination should focus on the organ or system suspected to be the source of bleeding. A thorough chest, abdomen, pelvis, and extremities examination is necessary if trauma is suspected. This examination may involve assessing for signs of injury. Additionally, imaging studies may be performed as clinically indicated to further evaluate potential injuries or sources of bleeding. 

The presentation of hemorrhagic shock can be categorized into different stages based on the amount of blood loss and the associated clinical signs. The various stages are as follows:

  • Class I (<15% blood loss):
    • Mild tachycardia is usually the first sign.
    • Blood pressure remains within normal range.
    • The skin may start to feel cool to the touch.
  • Class II (15-30% blood loss):
    • Tachycardia continues, becoming more pronounced.
    • Tachypnea begins.
    • Pulse pressure decreases.
  • Class III (30-40% blood loss):
    • Tachycardia worsens, with a rapid and weak pulse.
    • The decrease in blood pressure becomes more significant.
    • Skin becomes cold and appears pale and mottled.
    • Urine output decreases significantly.
  • Class IV (>40% blood loss):
    • This stage is dangerous and carries a high mortality rate.
    • Tachycardia and decreased blood pressure continue to worsen and can lead to loss of consciousness.
    • The pulse can disappear if there is more than 50% blood loss.

The following additional findings can provide valuable information in assessing a patient with potential bleeding disorders or hemorrhage during a skin examination.

  • Flank ecchymosis (Grey-Turner sign): Bruising in the flank area can indicate retroperitoneal hemorrhage.
  • Umbilical ecchymosis (Cullen sign): The appearance of bruising around the umbilicus can suggest intraperitoneal or retroperitoneal bleeding.
  • Jaundiced, yellow skin: Jaundice can indicate liver disease, certain hemoglobinopathies, or other forms of hemolysis.
  • Purpura and petechiae: The presence of purpura or petechiae can suggest platelet disorders or abnormalities in blood clotting.
  • Hemarthrosis: Its presence can indicate a bleeding disorder such as hemophilia.
  • Diffuse bleeding from intravenous (IV) sites and mucous membranes: This may be a sign of disseminated intravascular coagulation (DIC).


To determine the etiology and severity of the bleeding, a further diagnostic workup is crucial, which is as indicated below:

  • Blood typing and cross-matching: sending a blood sample immediately to the laboratory for typing and cross-matching allows for the preparation of blood products if transfusion is required. 
  • Complete blood count (CBC): A CBC provides essential information about the patient's red blood cell count, hemoglobin, and hematocrit levels. This helps assess the extent of blood loss and the severity of anemia. It is important to note that in an actively bleeding patient, the initial hematocrit level may not accurately reflect the true blood loss, as dilutional effects can temporarily maintain normal levels.
  • Serial CBCs: Monitoring serial CBCs is essential in cases of acute bleeding. This helps track changes in hemoglobin and hematocrit levels over time.
  • Mean corpuscular volume (MCV): A useful parameter for classifying anemia into different types. 
    • Microcytic anemias (MCV <80 fL) are characterized by small red blood cells. The mnemonic TAILS can help remember the common causes:
      • Thalassemia
      • Anemia of chronic disease
      • Iron deficiency anemia
      • Sideroblastic anemia/sickle cell disease
    • Normocytic anemias (MCV 80 to 100 fL) are characterized by normal-sized red blood cells. Causes include:
      • Active bleeding
      • Hemolysis
      • Malignancy
    • Macrocytic anemias (MCV >100 fL) are characterized by large red blood cells. Causes include:
      • Alcohol-related anemia
      • Folate deficiency
      • Vitamin B-12 deficiency
      • Some preleukemic conditions
  • LDH, haptoglobin, bilirubin: In hemolytic anemia, LDH and indirect bilirubin levels are elevated, while haptoglobin levels are low.
  • Blood urea nitrogen (BUN): Elevated BUN levels are commonly seen in patients with upper GI bleeds due to undigested blood.
  • Reticulocyte count: An increased reticulocyte count indicates an erythropoietic response by the bone marrow, suggesting active red blood cell production. A low reticulocyte count may mean an inadequate bone marrow response in conditions such as aplastic anemia, hematologic cancers, drugs, or toxins. Reticulocytosis correlates with an increased MCV in the blood count.
  • Screening labs for DIC: Screening tests include prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, fibrin split products, and platelet count. Findings associated with DIC include increased coagulation times, decreased platelets and fibrinogen levels, and fibrin split products.
    • DIC should be a diagnostic consideration in patients with severe sepsis, complications with giving birth, burns, malignancies, or uncontrolled hemorrhage.

In addition to the previously mentioned tests, the following tests can be considered in evaluating anemia. 

  • Iron studies
  • Folate and vitamin B-12 levels
  • Lead levels
  • Hemoglobin electrophoresis
  • Factor deficiency tests
  • Bleeding time
  • Bone marrow aspiration
  • Coombs test

Imaging studies play a crucial role in evaluating anemia and identifying the source of bleeding. Some common imaging modalities and procedures used in this context include the following:

  • Ultrasound is a quick and noninvasive tool for diagnosing intraperitoneal bleeding. In trauma settings, focused abdominal sonography for trauma (FAST) examination is often performed to assess for intra-abdominal hemorrhage, especially in unstable patients.
  • Chest X-ray is helpful in trauma patients to identify potential sources of bleeding such as hemothorax, pulmonary contusions, aortic rupture, or free air under the diaphragm associated with gastrointestinal bleeding.
  • Computed Tomography (CT) scanning is beneficial in patients with GI trauma or suspected GI bleeding.
  • Esophagogastroduodenoscopy (EGD) is commonly employed for diagnostic and therapeutic purposes in cases of upper GI bleeding. 
  • Sigmoidoscopy or colonoscopy are valuable tools for diagnosing and sometimes treating lower GI bleeding. 

Treatment / Management

Initial Management

  • Evaluate the ABCs (Airway, Breathing, and Circulation)
  • Treat any life-threatening conditions immediately
  • Administer supplemental oxygen
  • Establish 2 large-bore intravenous (IV) lines
  • IV fluid resuscitation (crystalloid is the initial fluid of choice) 
  • Apply direct pressure to any hemorrhage if possible 


The primary treatment for acute anemia is the administration of packed red blood cells (pRBCs) to replace the lost blood. Each unit of pRBCs is expected to increase the hematocrit by approximately 3 points.

  • Transfusion thresholds
    • A restrictive transfusion strategy is generally followed for hospitalized, hemodynamically stable adult patients, including critically ill patients. Transfusion is not recommended until the Hgb concentration is 7 g/dL or lower.[13] 
    • In patients with acute coronary syndrome, transfusion should be considered when the Hgb level is equal to or less than 8 g/dL.[14]
    • If the patient is actively bleeding, transfusion should be guided by the clinical situation and the severity of the bleeding. In cases of ongoing hemorrhage, a more liberal transfusion approach may be necessary to maintain hemodynamic stability until the source of bleeding is controlled.
    • A massive transfusion protocol may be initiated in massive hemorrhages, such as trauma or major surgical procedures. This protocol involves rapidly administering blood products, including pRBCs, fresh frozen plasma, platelets, and sometimes cryoprecipitate, to maintain hemodynamic stability and replace coagulation factors.
  • (B3)

In addition to packed red blood cells (pRBCs), other blood components can be utilized to treat specific conditions associated with acute anemia. These include platelets, fresh frozen plasma (FFP), and cryoprecipitate. Pharmacological options may also be considered in some instances. Here are further details on these treatment options: 

  • Blood products
    • Platelet transfusion is indicated in cases of thrombocytopenia or platelet dysfunction. Each unit of platelets raises the platelet count by approximately 10,000/microliters. Platelet transfusion is typically administered to prevent or control bleeding in patients with significant platelet deficiencies.
    • Fresh frozen plasma (FFP) is a blood product that contains all the coagulation factors. It is used to replenish depleted clotting factors in patients with coagulopathies. FFP is indicated in managing bleeding associated with deficiencies of multiple clotting factors or in patients who require rapid correction of coagulation abnormalities.
    • Cryoprecipitate is a blood component rich in fibrinogen, factor VIII, von Willebrand factor (vWF), and factor XIII. It primarily treats specific bleeding disorders, such as hemophilia A, von Willebrand disease, or fibrinogen deficiency. Cryoprecipitate is administered to replace specific clotting factors that are deficient or dysfunctional.
  • Pharmacological options
    • Vasopressor medications, such as norepinephrine or dopamine, increase blood pressure and cause vasoconstriction. They manage hypovolemic shock and conditions associated with significant blood loss.
    • Gastric acid inhibitors (H2-receptor antagonists) medications, such as ranitidine or famotidine, are used to reduce gastric acid secretion and aid in healing gastric and duodenal ulcers, which can cause upper gastrointestinal bleeding.
    • Glucocorticoid medications, such as prednisone, treat certain forms of autoimmune hemolytic anemias. They help suppress the immune response and decrease the destruction of red blood cells.
    • Vitamin K is administered to patients with liver disease or on certain medications (such as anticoagulants) to correct coagulation abnormalities. It helps replenish vitamin K-dependent clotting factors, including factors VII, IX, and X.

Sickle Cell Anemia

Treatment options for sickle cell anemia aim to manage the symptoms, prevent complications, and improve overall quality of life. A blood transfusion may be initiated based on the rate of hemoglobin decline and the patient's clinical condition. It is essential during aplastic crises characterized by low reticulocyte counts. An exchange transfusion may be performed in vaso-occlusive crises or severe complications, such as acute chest syndrome or stroke. This procedure involves gradually removing and replacing the patient's blood with a donor or a substitute. The goal is to reduce the number of sickle cells and lower blood viscosity, improving circulation and reducing the risk of further complications.

Hydroxyurea is an oral medication that can be used to manage sickle cell anemia. It works by stimulating fetal hemoglobin production, inhibiting the sickling of red blood cells. Hydroxyurea can help reduce the frequency and severity of sickle cell crises, decrease the need for transfusions, and improve overall symptoms and quality of life.

Platelet Disorders

Patients with thrombocytopenia accompanied by clinical evidence of bleeding should receive a platelet transfusion. Patients with platelet count lower than 10,000/μL are at risk for spontaneous cerebral hemorrhage and thus require a prophylactic transfusion. Large-volume plasmapheresis with FFP replacement is the preferred treatment for HUS and TTP. Many patients will require daily plasmapheresis. The treatment goals include increasing platelet count, decreasing lactate dehydrogenase (LDH), and reducing RBC fragments, which serve as positive indicators of treatment response. To complement plasmapheresis, many patients also receive high-dose glucocorticoids and antiplatelet agents (ie, aspirin). When patients respond poorly to plasmapheresis, interventions such as splenectomy or immunosuppression may be considered.

In the case of atypical HUS (aHUS), the initial management involves supportive care, similar to the approach used for Shiga Toxin-producing Escherichia Coli–associated HUS (STEC-HUS). However, for patients with severe complement-mediated HUS who are at risk of death or end-stage renal disease (ESRD), eculizumab, a humanized monoclonal antibody to C5, is recommended. Evidence suggests that early initiation can improve renal and nonrenal recovery.

The goal of the treatment of ITP is to maintain a safe platelet count that prevents clinically significant bleeding rather than normalizing the platelet counts. Bleeding risk is highest when the platelet counts are less than 10,000/microL. Immediate platelet transfusion is recommended for patients experiencing severe bleeding, such as intracranial or GI bleeding, and having a platelet count of less than 30,000/μL. In addition to platelet transfusion, specific therapies for ITP, including intravenous immune globulin (IVIG), glucocorticoids, and romiplostim, are recommended.

Congenital Bleeding Disorders

Von Willebrand disease, a bleeding disorder caused by deficient or defective von Willebrand factor, can be treated using different approaches. The primary treatment options for von Willebrand disease include desmopressin (DDAVP), recombinant von Willebrand factor (rVWF), and von Willebrand factor/factor VIII (vWF/FVIII) concentrates.

To treat hemophilia A (deficiency of factor VIII) and hemophilia B (deficiency of factor IX), factor VIII and IX concentrates are used, respectively. The dosage and administration of these concentrates depend on the site and severity of bleeding in each patient.

Disseminated Intravascular Coagulation (DIC)

The management of DIC primarily focuses on addressing the underlying cause to eliminate the stimulus for ongoing coagulation and thrombosis. When the platelet count remains above or equal to 10,000/μL, prophylactic transfusion of platelets and coagulation factors is not recommended. Treatment is warranted in patients with severe bleeding, those at high risk for bleeding complications, or those who require invasive procedures. Antifibrinolytic agents, such as tranexamic acid (TXA), epsilon-aminocaproic acid (EACA), or aprotinin, are contraindicated in managing DIC.

Differential Diagnosis

The following conditions should not be overlooked when evaluating patients presenting with anemia. 

  • Trauma: history of trauma or blood loss
  • GI bleed: history of GI bleeding, nonsteroidal anti-inflammatory drug (NSAID) or corticosteroid use, Aalochol use, cirrhosis, anticoagulant use
  • Rupture of vascular aneurysm: may present with sudden-onset tearing pain. Loss of consciousness may also occur.

In addition to the previously mentioned causes of anemia, it is essential to consider the following potential underlying factors:

  • Surgery: recent surgery involving moderate blood loss, history of bleeding disorders or excessive bruising, use of antibiotics
  • Menorrhagia: excessive menstrual bleeding lasting greater than 7 days
  • Nutritional deficiencies/malnutrition: iron deficiency, vitamin B12, or folate deficiency 
  • Myelodysplastic syndrome: macrocytic anemia with leukopenia, macro-ovalocytes, and especially bilineage cytopenias. 
  • Leukemia: acute leukemias present with pancytopenia and the presence of 20% blasts on peripheral smear; chronic leukemias can cause normocytic anemia
  • Infiltration of bone marrow by malignancy: weight loss, malaise, fevers, fatigue
  • Drug toxicity: known or suspected ingestion of causative drug before the onset
  • Anemia of chronic disease: history of known chronic inflammatory, autoimmune, or infectious states
  • Chronic kidney disease or chronic liver disease 
  • Pregnancy: most notable in the later stages, such as the third semester 


The prognosis of acute anemia is proportional to its severity, how rapidly it develops, and concurrent illnesses.[15][16][17][18][19] In general, anemia worsens the overall condition of a patient. When acute anemia occurs, it adds additional stress to the body, which can worsen preexisting diseases or conditions and potentially accelerate the progression of the underlying illness.

Time plays a critical role in the management of acute anemia. Delay or failure to promptly identify and address the underlying cause can have severe consequences and may lead to a rapid deterioration of the patient's health.


The most severe complication of acute anemia arises from hypovolemic shock caused by significant hemorrhage. Due to the decrease in blood volume, tissue hypoxia can occur, resulting in end-organ damage. This can manifest as a heart attack, heart failure, renal failure, acute hypoxic respiratory failure, or other forms of end-organ damage.    


In the management of challenging-to-manage anemias, leukemia patients, or severe cases of immune thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), or hemolytic uremic syndrome (HUS), the expertise of a Hematology Oncology specialist is essential.

Consultation with a gastroenterologist is essential for gastrointestinal (GI) bleeding cases. They can employ techniques such as endoscopy to visualize and treat bleeding lesions or ulcers in the GI tract, contributing to the effective management of GI bleeding.

In instances of trauma or rupture of a vascular aneurysm, the involvement of a surgeon is crucial. They can perform necessary surgical interventions to control bleeding, repair damaged blood vessels, and provide appropriate surgical care to patients in critical conditions.

Deterrence and Patient Education

Chronic anemia can often be a silent condition, with the body gradually adjusting to the lower levels of RBCs and Hgb. On the other hand, in acute cases of anemia, the signs and symptoms may be more pronounced, linking them to the underlying etiology. However, in the acute setting, time becomes a critical factor, as the healthcare practitioner must swiftly identify and address the cause to prevent further complications.

Collaboration and teamwork among the healthcare staff are crucial when managing anemia. Equally important is the cooperation and compliance of the patient.

Pearls and Other Issues

A summary of key facts when assessing and treating acute anemia are as follows:

  • Acute anemia occurs when there is an abrupt decrease in RBCs, and it is most commonly caused by hemolysis or acute hemorrhage.
  • Prioritize the ABCs (Airway, Breathing, Circulation) and start resuscitation.
  • Immediately obtain a blood sample for typing and cross-matching, and serial CBCs to monitor the hemoglobin and hematocrit levels over time.
  • Initial management includes providing supplemental oxygen, establishing large bore IV access, initiating intravenous (IV) fluid resuscitation (crystalloid is the initial fluid of choice), and applying direct pressure to a hemorrhage
  • Transfusion of pRBCs should be considered when Hgb levels are less than 7 g/dL or based on clinical indications. Each unit of pRBCs is expected to raise the hematocrit by approximately 3 percentage points and the Hgb level by 1 g/dL.

Enhancing Healthcare Team Outcomes

The interprofessional team is crucial in managing acute anemia to improve outcomes. Education becomes a vital component of the care plan with a focus on patient compliance with prescribed medications, such as iron supplements and steroids; avoidance of known triggers, such as alcohol consumption and NSAID use; and patient understanding of the underlying cause of the anemia to prevent future episodes.

The prognosis of acute anemia is highly variable and largely dependent on the specific cause. However, early stabilization and prompt initiation of appropriate treatment are associated with a better prognosis. Timely intervention can address the underlying cause, restore adequate blood volume and oxygen-carrying capacity, and prevent further complications. Through coordinated interprofessional care, including timely diagnosis, proper management, and patient education, healthcare providers can optimize outcomes and improve the prognosis for individuals with acute anemia.



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