Back To Search Results

Acute Anemia

Editor: Ajay Tambe Updated: 5/1/2024 12:34:04 AM


Anemia is characterized by a deficiency in the number of circulating red blood cells (RBCs), the amount of hemoglobin, or the volume of packed RBCs, known as hematocrit.[1] The World Health Organization (WHO) 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 anemia involves a sudden and rapid decrease in RBCs, typically caused by hemolysis or acute hemorrhage.
  • Chronic anemia is characterized by a gradual decline in RBCs over time. Its causes are varied and may include conditions such as iron or other nutritional deficiencies, chronic diseases, drug-induced factors, and other underlying health issues.


Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care


Anemia can result from various events and underlying conditions. Blood loss is among the most prevalent causes, resulting in decreased RBCs. This occurrence is widespread in cases of acute anemia observed in emergency room settings. Emergent conditions leading to acute anemia include traumatic injury causing arterial bleeding, ruptured aneurysms, massive upper or lower gastrointestinal (GI) hemorrhages, ruptured ectopic pregnancies, and disseminated intravascular coagulation (DIC).

Hemolytic anemias can also contribute to acute and chronic anemia, characterized by the destruction or reduced survival of RBCs. They are typically classified into 2 main categories: intracorpuscular and extracorpuscular. 

Intracorpuscular Hemolytic Anemias

Intracorpuscular hemolytic anemias encompass conditions where the defect or issue originates within the RBC itself. These abnormalities can involve defects in the RBC's membrane, enzymes, or hemoglobin molecules, leading to premature cell breakdown and subsequent anemia.

Hemoglobinopathies affect the structure or function of hemoglobin.

  • Sickle cell disease arises from a point mutation in the beta-globin chain's DNA, producing abnormal hemoglobin known as hemoglobin S (Hgb S). Under oxidative stress conditions, the Hgb S molecules polymerize and cause the RBCs to assume a sickle shape, which is less flexible and can block blood vessels, leading to tissue damage, pain crises, and other complications.
  • Thalassemias involve reduced alpha or beta globin chain production, leading to imbalanced hemoglobin synthesis. Due to the abnormal structure or function of hemoglobin, these conditions can cause various complications, including tissue damage and pain crises. 

Enzymopathies refer to conditions characterized by abnormalities in specific enzymes within RBCs (see Table. Enzymopathies Causing Hemolytic Anemia). These enzyme defects can disrupt normal cellular processes and lead to various clinical manifestations, including hemolysis and anemia.

Table 1. Enzymopathies Causing Hemolytic Anemia

Hemolytic Anemia Condition Abnormality
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
  • X-linked
  • Affects pentose pathway
  • Hemolysis is often triggered by external factors such as certain medications, infections, or exposure to oxidative stress
Hemophilia A
  • X-linked
  • Factor VIII deficiency
  • Causes prolonged bleeding after injuries or surgeries.
Pyruvate kinase (PK) deficiency
  • Autosomal recessive
  • Deficiency of the PK enzyme
  • Leads to nonspherocytic anemia

Phosphofructokinase (PFK) deficiency

(Known as Glycogen storage disease or Glycogenesis Type VII)

  • Autosomal Recessive
  • Deficiency of PFK
  • May experience muscle pain, rhabdomyolysis, and hemolytic anemia
Phosphoglycerate kinase (PGK) deficiency
  • X-linked 
  • Deficiency of PGK enzyme
  • Causes myopathy, splenomegaly, central nervous system disturbances
  • Leads to nonspherocytic hemolytic anemia
Aldolase deficiency
  • Autosomal recessive
  • Deficiency of aldolase enzyme
  • Causes muscle weakness
Triosephosphate isomerase (TPI) deficiency
  • Autosomal recessive
  • Various symptoms: anemia, intellectual disability, cardiomyopathy, and increased susceptibility to infections

Membrane-cytoskeletal defects

  • Hereditary spherocytosis
  • Hereditary elliptocytosis
  • Affects the RBC membrane and cytoskeleton
  • Result in the disfigurement of RBCs, leading to the removal of the spleen [3][4][5] 

Paroxysmal nocturnal hemoglobinuria (PNH)

  • Acquired disorder
  • Clonal autoimmune mechanism that leads to hemolysis, thrombosis, and marrow aplasia

Extracorpuscular Hemolytic Anemias

Extracorpuscular hemolytic anemias are a group of disorders where the defect leading to RBC destruction originates outside the RBC itself. These conditions typically involve factors in the bloodstream or external to the RBCs that cause their premature destruction.

Mechanical destruction (microangiopathic):

  • Thrombotic thrombocytopenic purpura (TTP) is characterized by the formation of platelet-rich thrombi in small blood vessels, primarily caused by a deficiency in ADAMTS13, metalloprotease responsible for cleaving von Willebrand factor. The classic triad of TTP includes microangiopathic hemolytic anemia, severe thrombocytopenia, and organ ischemia.[6]
  • Familial (atypical) hemolytic-uremic syndrome (HUS) results from gene mutations encoding complement regulatory proteins, leading to complement system dysregulation, immune system activation, and damage to small blood vessels. HUS also presents with a triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure, though its lesions are primarily confined to the kidneys, distinguishing it from TTP.[7][8][7]

Complement-mediated thrombotic microangiopathy is defined by the abnormal activation of the complement system, resulting in the formation of small blood clots within the microvasculature. This phenomenon can manifest in various disorders, including HUS.

Immune thrombocytopenic purpura is a condition in which IgG autoantibodies bind to platelets, marking them for destruction by the spleen. Consequently, platelet count decreases, raising the risk of bleeding, particularly when platelet levels plummet significantly.

Disseminated intravascular coagulation is characterized by widespread systemic activation of coagulation throughout the body in response to various underlying causes, such as infections, severe trauma, or certain complications during pregnancy. DIC results in excessive formation of intravascular fibrin, causing thrombosis. However, as coagulation factors are consumed, bleeding complications can arise.[9]

Toxic agents and drugs can destroy RBCs and cause hemolysis. Exposure to substances such as hyperbaric oxygen (or 100% oxygen), certain medications (eg, methyldopa, nitrates, chlorates, methylene blue, dapsone, cisplatin), numerous aromatic (cyclic) compounds, and other chemicals (arsine, stibine, copper, and lead) can trigger this process.

Infectious causes of hemolytic anemia include malaria, the most prevalent worldwide, and in certain regions, infection with Shiga toxin-producing E. Coli O157:H7, which leads to HUS. Additionally, in specific clinical situations such as 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 occurs when IgG antibodies target and bind to RBCs, leading to their destruction by macrophages, resulting in hemolysis. The affected RBCs often assume a rigid and nonelastic spherical shape known as spherocytes, making them more prone to rapid destruction. This type of anemia can be associated with autoimmune diseases (eg, lupus), certain types of lymphomas and leukemias, or can be drug-induced. In many cases, the cause remains unidentified.[10]

Hypersplenism is characterized by splenomegaly, resulting in increased destruction of blood cells, including RBCs. In acute conditions, such as infections or other causes of hemolysis, the spleen removes more RBCs, exacerbating the loss.[11] When the rate of hypersplenic destruction surpasses the marrow's capacity to produce RBCs, the anemia becomes more severe.  


Anemia is a prevalent condition, affecting one-fourth of the general population. Its prevalence is even higher among hospitalized patients, with approximately 50% affected. Among older hospitalized patients, the rate of anemia can rise to as high as 75%. 

Data collected in 2000 from over 81,000 health plan members revealed varying rates of anemia across specific patient populations. Patients with chronic kidney disease exhibited the highest prevalence of anemia, at 34.5%. Anemia prevalence among patients with cancer was 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 HIV infection had a 10% prevalence of anemia.[12]   


Acute anemia typically arises from 2 common causes: hemolysis or hemorrhage, both of which lead to a sudden decrease in RBCs. When the decline in RBCs is rapid, a hemoglobin level of 7 to 8 g/dL often triggers symptoms, as the body has insufficient time to compensate and replenish the lost volume. Healthy individuals can typically tolerate up to a 20% loss of blood volume without significant symptoms due to reflex vasospasm and the redistribution of blood flow.

However, when blood loss surpasses this threshold, patients start exhibiting signs and symptoms of hypovolemia. Compensatory mechanisms, like the redistribution of blood flow, become inadequate to sustain blood pressure, resulting in clinical manifestations such as postural hypotension, altered mental status, cool and clammy skin, tachycardia, and hyperventilation.

In cases of acute hemorrhage, hemoglobin and hematocrit levels may initially appear normal because both RBCs and plasma are lost concomitantly. This discrepancy becomes evident once intravenous fluids restore or replenish the patient’s plasma volume.


When examining a peripheral blood smear under a microscope, specific findings can provide valuable insights into the underlying condition. Observations related to certain types of anemia are as follows:

  • Microangiopathic hemolysis: In conditions characterized by microangiopathic hemolysis, such as TTP, immune thrombocytic purpura (ITP), HUS, and DIC, a peripheral blood smear examination may reveal several abnormal RBC shapes. These abnormalities include helmet cells (schistocytes), fragmented RBCs, and other RBC fragments. Spherocytes (small, round RBCs lacking central pallor) may also be present in some cases.
  • Sickle cell disease: A hallmark finding in sickle cell disease is the presence of sickle-shaped cells, also known as sickle cells. These cells have a crescent or "sickle" shape due to the abnormal Hgb S in individuals with this genetic disorder. Another characteristic feature of 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 comprehensive yet focused medical history is essential for guiding further assessment and management. However, specific priorities should be addressed initially, including managing the patient's airway, breathing, and circulation (ABCs) are stable. If required, immediate resuscitation measures should be initiated to stabilize the patient.

In situations where the patient cannot communicate, obtaining as much information as possible from emergency medical services (EMS) personnel or individuals at the bedside is crucial. Additionally, reviewing previous medical charts, if available, can offer valuable insights into the patient's medical history and aid in understanding the underlying cause of anemia.

A focused history should also include identifying the potential source of bleeding. For example, if GI hemorrhage is suspected, obtaining a detailed GI history is essential, which may involve asking about any prior episodes of GI bleeding, symptoms of GI 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 Examination

In assessing a patient with anemia, regular monitoring of vital signs is essential to evaluate the patient's stability and response to interventions. As mentioned earlier, the initial physical examination should focus on the organ or system suspected to be the source of bleeding. If trauma is suspected, a thorough examination of the chest, abdomen, pelvis, and extremities is necessary, including assessing for signs of injury. Additionally, imaging studies may be conducted 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 typically include:

  • Class 1 (<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 2 (15%-30% blood loss):
    • Tachycardia continues, becoming more pronounced
    • Tachypnea begins
    • Pulse pressure decreases
  • Class 3 (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 4 (>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 >50% blood loss

Additional findings during a skin examination can offer valuable insights into assessing a patient with potential bleeding disorders or hemorrhage. These may include:

  • 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: Bleeding into joint spaces can indicate a bleeding disorder such as hemophilia.
  • Diffuse bleeding from intravenous sites and mucous membranes: This may be a sign of DIC.


A further diagnostic workup is crucial to determining the etiology and severity of the bleeding. This comprehensive assessment may include a range of tests and procedures to identify the underlying cause and extent of the hemorrhage.

Blood typing and cross-matching involve promptly sending a blood sample to the laboratory for typing and cross-matching. This facilitates the preparation of blood products if transfusion is necessary, ensuring compatibility and safety during transfusion procedures. 

Complete blood count (CBC) provides essential insights into the patient's RBC count, hemoglobin, and hematocrit levels, aiding in evaluating blood loss and the severity of anemia. However, it is essential to recognize that in actively bleeding patients, the initial hematocrit level may not accurately reflect the true extent of blood loss due to temporary dilutional effects maintaining normal levels.

Serial CBC monitoring is crucial in acute bleeding cases, as it allows for tracking changes in hemoglobin and hematocrit levels over time. This ongoing assessment helps clinicians gauge the effectiveness of interventions and the patient's response to treatment.

Mean corpuscular volume (MCV) is a valuable parameter used to classify anemia into different types based on the average volume of RBCs.

  • Microcytic anemias (MCV <80 fL) are identified by small RBCs. The mnemonic TAILS can help assist in recalling the common causes:
    • Thalassemia
    • Anemia of chronic disease
    • Iron deficiency anemia
    • Lead poisoning
    • Sideroblastic anemia/sickle cell disease
  • Normocytic anemias (MCV 80 to 100 fL) feature normal-sized RBCs. Causes encompass:
    • Active bleeding
    • Anemia of chronic disease
    • Hemolysis
    • Malignancy
  • Macrocytic anemias (MCV >100 fL) exhibit large RBCs. Causes include:
    • Alcohol-related anemia
    • Folate deficiency
    • Vitamin B-12 deficiency
    • Some preleukemic conditions

Lactate dehydrogenase (LDH), haptoglobin, and bilirubin can indicate hemolytic anemia with elevated LDH and indirect bilirubin levels and decreased haptoglobin levels.

Blood urea nitrogen (BUN) levels are commonly elevated in patients with upper GI bleeds due to undigested blood.

Reticulocyte count is increased due to an erythropoietic response by the bone marrow, suggesting active RBC production. Conversely, a low reticulocyte count may indicate an inadequate bone marrow response, as seen in conditions such as aplastic anemia, hematologic cancers, drugs, or toxins. Reticulocytosis often corresponds with an increased MCV in the blood count.

Screening labs for DIC typically include prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, fibrin split products, and platelet count. Diagnostic findings indicative of DIC comprise increased coagulation times, decreased platelets and fibrinogen levels, and fibrin split products. DIC should be considered in the diagnosis of patients experiencing severe sepsis, childbirth complications, burns, malignancies, or uncontrolled hemorrhage.

Additional studies for evaluating anemia include the following:

  • Folate and vitamin B12 levels
  • Lead levels
  • Hemoglobin electrophoresis
  • Factor deficiency tests
  • Bleeding time
  • Bone marrow aspiration
  • Coombs test

Imaging studies are vital for assessing anemia and identifying the source of bleeding. Common imaging modalities and procedures used for this purpose include:

  • Ultrasound: A quick and noninvasive tool for diagnosing intraperitoneal bleeding. In trauma settings, a focused abdominal sonography for trauma (FAST) examination is often performed to assess for intraabdominal hemorrhage, especially in unstable patients.
  • Chest x-ray: 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 GI bleeding.
  • Computed tomography scanning: Beneficial in patients with GI trauma or suspected GI bleeding.
  • Esophagogastroduodenoscopy: Commonly employed for diagnostic and therapeutic purposes in cases of upper GI bleeding. 
  • Sigmoidoscopy or colonoscopy: Valuable tools for diagnosing and sometimes treating lower GI bleeding. 

Treatment / Management

The treatment and management of acute anemia are paramount in stabilizing the patient and addressing the condition's underlying cause. Acute anemia requires prompt intervention to restore adequate oxygen delivery to tissues and prevent further complications. Treatment strategies often involve a combination of measures aimed at stopping ongoing bleeding, replacing lost blood volume, and addressing the underlying cause of the anemia. 

Initial Management

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


The primary treatment for acute anemia involves administering packed red blood cells (pRBCs) to replenish the lost blood volume. Typically, 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, those in critically care settings, with transfusion not recommended  until the hemoglobin concentration drops to 7 g/dL or lower.[13] However, in patients with acute coronary syndrome, transfusion consideration arises when hemoglobin level equals or falls below 8 g/dL.[14](B3)

For actively bleeding patients, transfusion decisions should be guided by clinical context and bleeding severity, with a more liberal approach potentially required to maintain hemodynamic stability during ongoing hemorrhage until bleeding control is achieved. In cases of massive hemorrhages, such as trauma or major surgical procedures, initiation of a massive transfusion protocol is warranted. This protocol involves promptly administering blood products, including pRBCs, fresh frozen plasma (FFP), platelets, and sometimes cryoprecipitate, to ensure hemodynamic stability and replenish coagulation factors.

All these blood components are integral to treating specific conditions associated with anemia. They may be considered in instances as outlined (see Table. Treatment Options for Acute Anemia): 

Table 2. Treatment Options for Acute Anemia

Blood Product Indication
  • Thrombocytopenia or platelet dysfunction
  • Typically administered to prevent or control bleeding in patients with significant platelet deficiencies
  • Each unit of platelets raises the platelet count by approximately 10,000 microliters
Fresh frozen plasma (FFP)
  • Blood products that contain all the coagulation factors
  • Replenishes depleted clotting factors in patients with coagulopathies
  • Rapidly corrects coagulation abnormalities
  • Rich in fibrinogen, factor VIII, von Willebrand factor (vWF), factor XIII
  • Hemophilia A, von Willebrand disease, fibrinogen deficiency
Pharmacologic Options  
  • Norepinephrine, dopamine
  • Increase blood pressure and cause vasoconstriction 
  • Used to manage hypovolemic shock and conditions with significant blood loss

 Gastric acid inhibitors 

(H2-receptor antagonists)

  • Ranitidine, famotidinene
  • Reduce gastric acid secretion
  • Aid in healing gastric and duodenal ulcers
Glucocorticoid medications 
  • Prednisone
  • Treat autoimmune hemolytic anemias
  • Help suppress the immune response and decrease the destruction of RBCs 
Vitamin K
  • Administered to patients with liver disease or on certain medications such as anticoagulants to correct coagulation abnormalities
  • Replenishes vitamin K-dependent clotting factors, including factors VII, IX, and X

Sickle cell anemia

Treatment options for sickle cell anemia focus on symptom management, complication prevention, and enhancing overall quality of life. A blood transfusion may be initiated based on the rate of hemoglobin decline and the patient's clinical condition, especially 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 replacing the patient's blood with a donor or substitute, aiming to decrease sickle cell count, reduce blood viscosity, enhance circulation, and reduce further complications.

Hydroxyurea, oral medication, is a viable option for managing sickle cell anemia. Its mechanism involves stimulating fetal hemoglobin production, thereby inhibiting the sickling of RBCs. Hydroxyurea effectively reduces the frequency and severity of sickle cell crises, decreases the need for transfusions, and improves overall symptoms and quality of life.

Platelet disorders

Patients with thrombocytopenia and clinical evidence of bleeding warrant a platelet transfusion. Those with platelet counts below 10,000/μL face a risk of spontaneous cerebral hemorrhage and thus necessitate prophylactic transfusion. For conditions like HUS and TTP, large-volume plasmapheresis with FFP replacement is the preferred treatment, often requiring daily sessions. Treatment objectives include increasing platelet count, decreasing lactate dehydrogenase (LDH) levels, and reducing RBC fragments as positive indicators of treatment response. Complementary measures, such as high-dose glucocorticoids and antiplatelet agents like aspirin, are often employed alongside plasmapheresis in cases of inadequate response to plasmapheresis interventions such as splenectomy or immunosuppression may be considered. 

Initial management of atypical hemolytic uremic syndrome (aHUS) 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, particularly those at risk of death or end-stage renal disease (ESRD), eculizumab, a humanized monoclonal antibody to C5, is recommended. Emerging evidence suggests that early initiation of eculizumab can improve renal and nonrenal recovery.

The primary objective in treating ITP is to maintain a safe platelet count that mitigates clinically significant bleeding, rather than normalizing platelet counts. The bleeding risk occurs when the platelet counts fall below 10,000/µL. 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 commonly used.

Congenital bleeding disorders

Von Willebrand disease, characterized by deficient or defective von Willebrand factor, can be effectively managed using different approaches. Primary treatment options include desmopressin (DDAVP), recombinant von Willebrand factor (rVWF), and von Willebrand factor/factor VIII (vWF/FVIII) concentrates. These treatments aim to replenish or enhance the function of von Willebrand factor, thereby mitigating bleeding episodes and improving overall clinical outcomes.

Factor VIII and IX concentrates are employed to manage hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency), respectively. The dosage and administration of these concentrates vary depending on the site and severity of bleeding in each patient. This tailored approach ensures effective control of bleeding episodes while minimizing the risk of complications associated with hemophilia.

Disseminated intravascular coagulation

The management of DIC primarily focuses on addressing the underlying cause to eliminate the stimulus for ongoing coagulation and thrombosis. Prophylactic transfusion of platelets and coagulation factors is not recommended when the platelet count remains above or equal to 10,000/μL. However, treatment is warranted in patients with severe bleeding, those at high risk for bleeding complications, or those requiring invasive procedures. Notably, 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
    • Trauma or blood loss
  • GI bleed
    • Noted GI bleed
    • Nonsteroidal anti-inflammatory drug (NSAID) or corticosteroid use
    • Alcohol use
    • Cirrhosis
    • Anticoagulant use
  • Rupture of vascular aneurysm
    • May present with sudden-onset tearing pain. Loss of consciousness may also occur.
  • Surgery
    • Recent surgery involving moderate blood loss
    • History of bleeding disorders or excessive bruising
    • Use of antibiotics
  • Menorrhagia
    • Excessive menstrual bleeding lasting >7 days
  • Nutritional deficiencies/malnutrition
    • Iron, 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 correlates with its severity, rate of development, and concurrent illnesses.[15][16][17][18][19] Typically, anemia exacerbates a patient's overall condition, adding further stress to the body and potentially accelerating the progression of underlying diseases or conditions. 

Time is of the essence in managing acute anemia. Failure to promptly identify and address the underlying cause can have severe consequences, potentially resulting in a rapid deterioration of the patient's health. Therefore, timely intervention and appropriate management are paramount to mitigate adverse outcomes associated with acute anemia. 


The most severe complication of acute anemia arises from hypovolemic shock caused by significant hemorrhage. Reduced blood volume can lead to tissue hypoxia, precipitating end-organ damage such as heart attack, heart failure, renal failure, acute hypoxic respiratory failure, or other manifestations of organ dysfunction.    


In the management of challenging-to-treat anemias, leukemia patients, or severe cases of ITP, TTP, or HUS, the expertise of a hematology/oncology specialist is essential. Their specialized knowledge and experience are crucial for accurately diagnosing and developing tailored treatment plans for these complex hematologic conditions.

Consultation with a gastroenterologist is essential for GI bleeding cases. Their expertise allows for using techniques like endoscopy to visualize and treat bleeding lesions or ulcers in the GI tract, significantly enhancing the management of GI bleeding.

A surgeon's involvement is crucial in instances of trauma or vascular aneurysm rupture. They possess the skill to execute essential surgical interventions, control bleeding, repair damaged blood vessels, and administer appropriate surgical care to patients in critical conditions.

Deterrence and Patient Education

Chronic anemia can manifest silently, with the body gradually adapting to lower RBC and hemoglobin levels. Conversely, acute anemia may present with more pronounced signs and symptoms, explaining the underlying cause. However, in acute scenarios, time becomes paramount as healthcare practitioners must promptly identify and address the cause to prevent potential complications.

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

Pearls and Other Issues

Key facts to keep in mind about acute anemia are as follows:

  • Acute anemia is a sudden decline in RBC count, typically precipitated by hemolysis or acute hemorrhage.
  • Acute anemia can result from various causes, including trauma, hemorrhage (such as GI bleeding or trauma-related bleeding), hemolysis (such as autoimmune hemolytic anemia or hemolytic transfusion reaction), and other acute conditions.
  • Patients with acute anemia may present with symptoms such as weakness, fatigue, pallor, tachycardia, hypotension, shortness of breath, and, in severe cases, shock.
  • In cases of acute anemia, it is crucial to prioritize the ABCs and initiate resuscitation as necessary.
  • Promptly collect a blood sample for typing and cross-matching and conduct serial CBCs to closely monitor hemoglobin and hematocrit levels throughout the patient's care.
  • The initial steps in management involve administering supplemental oxygen, establishing large-bore intravenous access, initiating intravenous fluid resuscitation with crystalloid fluids, and applying direct pressure to any site of hemorrhage to control bleeding.
  • Transfusion of pRBCs is indicated when hemoglobin levels drop below 7 g/dL or based on clinical judgment. Typically, each unit of pRBCs increases the hematocrit by about 3 percentage points and the hemoglobin level by 1 g/dL.
  • Complications of acute anemia include hypovolemic shock, tissue hypoxia, end-organ damage, and death if left untreated or inadequately managed. Early recognition and intervention are crucial to prevent adverse outcomes.

Enhancing Healthcare Team Outcomes

In the realm of acute anemia management, various healthcare professionals must collaborate effectively to ensure patient-centered care, optimal outcomes, and safety. Physicians, advanced practitioners, nurses, pharmacists, and other team members should possess proficient skills in recognizing anemia's signs and symptoms, conducting diagnostic tests, and implementing appropriate treatment strategies promptly.

Responsibilities are distributed among team members, with clear communication channels established to facilitate interprofessional collaboration and care coordination. Regular communication updates, shared decision-making, and mutual respect among team members enhance patient safety and contribute to improved outcomes.

The interprofessional team is pivotal in managing acute anemia to improve patient outcomes. Education is a vital component of the care plan, emphasizing patient adherence to prescribed medications like iron supplements and steroids, avoidance of known triggers such as alcohol consumption and NSAID use, and comprehension of the underlying cause of the anemia to prevent future episodes.



Vieth JT, Lane DR. Anemia. Hematology/oncology clinics of North America. 2017 Dec:31(6):1045-1060. doi: 10.1016/j.hoc.2017.08.008. Epub     [PubMed PMID: 29078923]


Cappellini MD, Motta I. Anemia in Clinical Practice-Definition and Classification: Does Hemoglobin Change With Aging? Seminars in hematology. 2015 Oct:52(4):261-9. doi: 10.1053/j.seminhematol.2015.07.006. Epub 2015 Jul 17     [PubMed PMID: 26404438]


Perrotta S, Gallagher PG, Mohandas N. Hereditary spherocytosis. Lancet (London, England). 2008 Oct 18:372(9647):1411-26. doi: 10.1016/S0140-6736(08)61588-3. Epub     [PubMed PMID: 18940465]


Iolascon A, Avvisati RA, Piscopo C. Hereditary spherocytosis. Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine. 2010 Sep:17(3):138-42. doi: 10.1016/j.tracli.2010.05.006. Epub 2010 Jul 23     [PubMed PMID: 20655264]


Niss O, Chonat S, Dagaonkar N, Almansoori MO, Kerr K, Rogers ZR, McGann PT, Quarmyne MO, Risinger M, Zhang K, Kalfa TA. Genotype-phenotype correlations in hereditary elliptocytosis and hereditary pyropoikilocytosis. Blood cells, molecules & diseases. 2016 Oct:61():4-9. doi: 10.1016/j.bcmd.2016.07.003. Epub 2016 Jul 17     [PubMed PMID: 27667160]


Joly BS, Coppo P, Veyradier A. Thrombotic thrombocytopenic purpura. Blood. 2017 May 25:129(21):2836-2846. doi: 10.1182/blood-2016-10-709857. Epub 2017 Apr 17     [PubMed PMID: 28416507]


Webster K, Schnitzler E. Hemolytic uremic syndrome. Handbook of clinical neurology. 2014:120():1113-23. doi: 10.1016/B978-0-7020-4087-0.00075-9. Epub     [PubMed PMID: 24365375]


Picard C, Burtey S, Bornet C, Curti C, Montana M, Vanelle P. Pathophysiology and treatment of typical and atypical hemolytic uremic syndrome. Pathologie-biologie. 2015 Jun:63(3):136-43. doi: 10.1016/j.patbio.2015.03.001. Epub 2015 Apr 3     [PubMed PMID: 25845294]


Levi M. Diagnosis and treatment of disseminated intravascular coagulation. International journal of laboratory hematology. 2014 Jun:36(3):228-36. doi: 10.1111/ijlh.12221. Epub     [PubMed PMID: 24750668]


Liebman HA, Weitz IC. Autoimmune Hemolytic Anemia. The Medical clinics of North America. 2017 Mar:101(2):351-359. doi: 10.1016/j.mcna.2016.09.007. Epub 2016 Dec 14     [PubMed PMID: 28189175]


Lv Y, Lau WY, Li Y, Deng J, Han X, Gong X, Liu N, Wu H. Hypersplenism: History and current status. Experimental and therapeutic medicine. 2016 Oct:12(4):2377-2382     [PubMed PMID: 27703501]


Nissenson AR, Wade S, Goodnough T, Knight K, Dubois RW. Economic burden of anemia in an insured population. Journal of managed care pharmacy : JMCP. 2005 Sep:11(7):565-74. doi: 10.18553/jmcp.2005.11.7.565. Epub     [PubMed PMID: 16137214]

Level 2 (mid-level) evidence


The Lancet Haematology. Updates on blood transfusion guidelines. The Lancet. Haematology. 2016 Dec:3(12):e547. doi: 10.1016/S2352-3026(16)30172-7. Epub     [PubMed PMID: 27890071]


Napolitano LM. Anemia and Red Blood Cell Transfusion: Advances in Critical Care. Critical care clinics. 2017 Apr:33(2):345-364. doi: 10.1016/j.ccc.2016.12.011. Epub     [PubMed PMID: 28284299]

Level 3 (low-level) evidence


Jiménez D, Escobar C, Martí D, Díaz G, César J, García-Avello A, Sueiro A, Yusen RD. Association of anaemia and mortality in patients with acute pulmonary embolism. Thrombosis and haemostasis. 2009 Jul:102(1):153-8. doi: 10.1160/TH09-01-0003. Epub     [PubMed PMID: 19572080]

Level 2 (mid-level) evidence


Migone de Amicis M, Chivite D, Corbella X, Cappellini MD, Formiga F. Anemia is a mortality prognostic factor in patients initially hospitalized for acute heart failure. Internal and emergency medicine. 2017 Sep:12(6):749-756. doi: 10.1007/s11739-017-1637-5. Epub 2017 Feb 23     [PubMed PMID: 28233161]


Kikuchi M, Inagaki T, Shinagawa N. Five-year survival of older people with anemia: variation with hemoglobin concentration. Journal of the American Geriatrics Society. 2001 Sep:49(9):1226-8     [PubMed PMID: 11559383]

Level 2 (mid-level) evidence


du Cheyron D, Parienti JJ, Fekih-Hassen M, Daubin C, Charbonneau P. Impact of anemia on outcome in critically ill patients with severe acute renal failure. Intensive care medicine. 2005 Nov:31(11):1529-36     [PubMed PMID: 16205892]


Cai YL, Wang SQ, Zhong HJ, He XX. The effect of anemia on the severity and prognosis of patients with acute pancreatitis: A single-center retrospective study. Medicine. 2022 Dec 30:101(52):e32501. doi: 10.1097/MD.0000000000032501. Epub     [PubMed PMID: 36596024]

Level 2 (mid-level) evidence