Acute Anemia

Etiology

Acute 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, surgical complications, and disseminated intravascular coagulation (DIC).[3]

Bone marrow suppression or failure can lead to acute anemia due to inadequate production of red blood cells. Conditions, eg, aplastic anemia, which may be triggered by factors like drug use or viral infections, result in a marked decrease in bone marrow activity. Additionally, acute leukemia and myelodysplastic syndromes can cause disruptions in normal blood cell production, leading to anemia. Severe infections or sepsis can also temporarily suppress the bone marrow, further exacerbating the anemia by reducing the body's ability to produce new red blood cells.

Inflammation accompanying several medical conditions has been shown to cause an acute, reversible drop in hematologic parameters.[4][5] The mechanism involves hepcidin, which is an acute-phase reactant. Inflammatory mediators (eg, cytokines, IL6, IL1, IL22, TNF alpha, and IFN gamma) cause an increase in hepcidin levels, leading to a decrease in ferroportin with a subsequent decrease in iron absorption (via the GI tract) and release of stored iron via tissue iron receptors. Treatment and resolution of the disease-causing inflammation resolves the underlying anemia. Anemia of chronic disease is a consequence of a chronic elevation of hepcidin. The 4 "I's" of inflammation, infection, ischemia, and infarction can elevate the hepcidin level. 

Hemolytic Anemias

Hemolytic anemias, characterized by the destruction or reduced survival of RBCs, also contribute to acute and chronic anemia. Hemolytic anemia is typically subclassified 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. The following abnormalities can involve defects in the RBC's membrane, enzymes, or hemoglobin molecules, leading to premature cell breakdown and subsequent anemia:

• Hemoglobinopathies: These conditions involve hemoglobin structure or function impairment.
  • 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 severe anemia, iron overload leading to heart, liver, and endocrine dysfunction, bone deformities, splenomegaly, increased infection risk, and delayed growth. 
• Enzymopathies: These conditions are characterized by abnormalities in specific enzymes within RBCs (see Table 1. Enzymopathies Causing Hemolytic Anemia), which can disrupt normal cellular processes and lead to various clinical manifestations, including hemolysis and anemia

Table 1. Enzymopathies Causing Hemolytic Anemia

• RBC membrane-cytoskeletal defects: Hereditary spherocytosis and elliptocytosis are some conditions that involve these types of RBC abnormalities, resulting in the disfigurement of RBCs, leading to the removal of the spleen.[6][7][8] Hereditary spherocytosis causes hemolytic anemia, jaundice, splenomegaly, gallstones, and spherocytes on a peripheral smear with increased osmotic fragility. Hereditary elliptocytosis causes mild to severe hemolytic anemia, jaundice, splenomegaly, and elliptical (oval-shaped) RBCs on a peripheral smear, with most cases being asymptomatic. Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired RBC membrane defect caused by a mutation in the PIGA gene in hematopoietic stem cells, leading to the absence of cell surface markers CD55 and CD59. This clonal defect leads to intravascular hemolysis, dark-colored urine (especially in the morning), anemia, fatigue, abdominal pain, thrombosis, and recurrent infections.

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, including:

• Mechanical destruction or microangiopathic hemolytic anemia (MAHA): This is a type of anemia characterized by the destruction of red blood cells in small blood vessels due to mechanical injury from microthrombi formation, often associated with conditions like Thrombotic thrombocytopenic purpura (TTP), hemolytic-uremic syndrome (HUS), or DIC.
  • 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 pentad of TTP consists of thrombocytopenia, microangiopathic hemolytic anemia, neurological symptoms, fever, and renal dysfunction. Not all patients present with the full pentad, and some may have only a subset of these symptoms.[9]
  • HUS is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, often triggered by an infection with Shiga toxin-producing bacteria (eg, E. coli).

• Complement-mediated thrombotic microangiopathy: This disorder 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 atypical HUS, which also presents with a triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure, though renal involvement is more severe as compared to TTP.[10][11]

• Disseminated intravascular coagulation: DIC 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.[12]

• Toxic agents and drugs: Hemolysis can also be caused by toxic substances and drugs destroying RBCs. Exposure to substances, eg, hyperbaric oxygen (or 100% oxygen), certain medications (eg, methyldopa, nitrates, chlorates, methylene blue, dapsone, and cisplatin), numerous aromatic (cyclic) compounds, and other chemicals (eg, arsine, stibine, copper, and lead) can trigger this process.

• Infection: The most prevalent infectious cause of hemolytic anemia is malaria, which is transmitted through the bloodstream. In certain regions, infection with Shiga toxin-producing E. coli O157:H7 leads to HUS. Additionally, in specific clinical situations (eg, open wounds, septic abortions, or contaminated blood transfusions), Clostridium perfringens sepsis can induce life-threatening hemolysis through the action of a toxin with lecithinase activity.

• Autoimmune conditions: 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 non-elastic 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.[13]
• Hypersplenism: This condition is characterized by splenomegaly, resulting in increased destruction of blood cells, including RBCs. In acute conditions, eg, infections or other causes of hemolysis, the spleen removes more RBCs, exacerbating the loss.[14] When the rate of hypersplenic destruction surpasses the marrow's capacity to produce RBCs, the anemia becomes more severe.  

Epidemiology

Anemia is a prevalent condition, affecting 25% of the general population; however, the prevalence of severe anemia is relatively lower at 0.9%.[CDC Anemia Prevalence 2021 to 2023] Anemia is more common among hospitalized patients, with approximately 50% affected.[15] Among older hospitalized patients, the rate of anemia can rise to as high as 80%.[16] 

Acute anemia is most commonly observed in populations undergoing substantial blood loss from events including trauma, surgery, childbirth, or heavy menstrual bleeding, with a higher prevalence in women of reproductive age. Acute anemia is of particular concern in areas with high malnutrition and iron deficiency rates, especially among young children, pregnant women, and older adults. Hemorrhage remains the most frequent cause of acute anemia.

Pathophysiology

Acute anemia typically arises from hemolysis or hemorrhage, the 2 most common causes, both of which lead to a sudden decrease in RBCs. When RBCs are rapidly reduced, 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, eg, 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. Administering intravenous fluids can have a dilutional effect, making the anemia more pronounced.

Histopathology

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, HUS, and DIC, a peripheral blood smear examination may reveal several abnormal RBC shapes. These abnormalities include helmet cells, fragmented RBCs (schistocytes), and other RBC fragments.

• Autoimmune hemolytic anemias or hereditary spherocytosis: Spherocytes (small, round RBCs lacking central pallor) may be present in some cases.

• Sickle cell disease: A hallmark finding in sickle cell disease is the presence of sickle-shaped red blood 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 these individuals due to functional asplenia or hyposplenism. 

History and Physical

Clinical History

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 immediately, including managing the patient's ABCs are stable. If required, immediate resuscitation measures should be initiated to stabilize the patient. Please see StatPearls' companion resource, "Trauma Primary Survey", for further information on performing an ABC survey.

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. Note any medical alert devices (ie, necklaces).

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 acute 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, including:

• Flank ecchymosis (Grey-Turner sign): Bruising in the flank area can indicate retroperitoneal hemorrhage often due to trauma, ruptured aneurysms, or other internal bleeding sources.
• Umbilical ecchymosis (Cullen sign): The appearance of bruising around the umbilicus can suggest intraperitoneal or retroperitoneal bleeding commonly seen in conditions like ruptured ectopic pregnancy.
• Jaundiced, yellow skin: Jaundice can indicate liver disease, certain hemoglobinopathies (eg, sickle cell disease), or other causes of hemolysis, indicating elevated bilirubin levels. 
• 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. 

Evaluation

A detailed diagnostic workup is crucial to determining the etiology and severity of the bleeding. A thorough assessment includes a range of tests and procedures to identify the underlying cause and extent of hemorrhage.

Laboratory Studies

Blood typing and cross-matching involve promptly sending a blood sample to the laboratory to facilitate the preparation of blood products if transfusion is necessary, ensuring compatibility and safety during transfusion procedures. A 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, recognizing 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 is essential. Additionally, 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 acute anemia into different types based on the average volume of RBCs. Note that a "reactive thrombocytosis" can present with an iron deficiency, and serum ferritin (a measure of iron storage) may be of dubious help since ferritin is a phase reactant protein and can be falsely elevated in the setting of inflammation. MCV subtypes and their associated etiologies include:

• Microcytic anemias (MCV <80 fL), identified by small RBCs
  • Thalassemia
  • Iron deficiency anemia
  • Lead poisoning
  • Sideroblastic anemia

• Normocytic anemias (MCV 80 to 100 fL) feature normal-sized RBCs
  • Active bleeding
  • Hemolysis
  • Malignancy

• Macrocytic anemias (MCV >100 fL) exhibit large RBCs.
  • Alcohol-related anemia
  • Folate deficiency
  • Vitamin B-12 deficiency
  • Myelodysplastic syndrome
  • Hypothyroidism

Lactate dehydrogenase (LDH), haptoglobin, and bilirubin can indicate hemolytic anemia, with elevated LDH, indirect bilirubin, and decreased haptoglobin levels. Blood urea nitrogen (BUN) levels are commonly elevated in patients with upper GI bleeds due to undigested blood. An increased reticulocyte count may be noted secondary 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, and drug or toxin exposures. Reticulocytosis often corresponds with an increased MCV in the blood count.

Screening laboratory studies 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 the presence of fibrin split products (eg, D-dimer). 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 biopsy and aspiration
• Coombs test

Diagnostic Imaging and Procedures

Imaging studies are vital for assessing acute 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, which is associated with GI bleeding.

• Computed tomography scanning: Beneficial in patients with 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 require prompt intervention to restore adequate oxygen delivery to tissues and prevent further complications. Treatment strategies often involve a combination of measures to stop ongoing bleeding, replace lost blood volume, and address the underlying cause of the anemia. 

Initial Management for Acute Bleeding

The initial management of hemorrhage involves resuscitation and rapid blood volume replacement as clinically indicated until the patient is stabilized. Please see StatPearls' companion resource, "Hypovolemic Shock," for further information on the acute hemorrhage management. In general, this includes:

• Evaluating the ABCs 
• Treating any life-threatening conditions immediately
• Administering supplemental oxygen
• Establishing 2 large-bore intravenous lines
• Intravenous fluid resuscitation (crystalloid is the initial fluid of choice) 
• Applying direct pressure to any hemorrhage site, if possible 

Acute Anemia Treatment 

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 and the hemoglobin level by roughly 1 point.

Transfusion thresholds

A restrictive transfusion strategy is generally followed for hospitalized, hemodynamically stable adult patients and those in critical care settings, with transfusion not recommended until the hemoglobin concentration drops to 7 g/dL or lower.[17] However, in patients with acute coronary syndrome, transfusion consideration arises when the hemoglobin level is ≤8 g/dL.[18] At very low hemoglobin concentrations (eg, 3 g/dL), the body’s oxygen needs cannot be met, and tissue hypoxia occurs.[19](B3)

For actively bleeding patients, transfusion decisions should be guided by clinical context and bleeding severity. A more liberal approach may be required to maintain hemodynamic stability until bleeding control is achieved during ongoing hemorrhage. 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 acute anemia. They may be considered for certain clinical indications (see Table 2. Treatment Options for Acute Anemia).

Table 2. Treatment Options for Acute Anemia

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, eg, 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, an 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 LDH levels, and reducing RBC fragments as positive indicators of treatment response. Complementary measures, including corticosteroids and rituximab (a monoclonal antibody) are also often used to treat autoimmune TTP. Immunosuppressants such as cyclophosphamide and rarely splenectomy may be considered in chronic or relapsed TTP, especially when plasmapheresis and other treatments are not effective.

Initial management of atypical hemolytic uremic syndrome (aHUS) involves supportive care and plasmapheresis similar to the approach used for TTP. However, for patients with severe complement-mediated HUS, particularly those at risk of death or end-stage renal disease, 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 immune thrombocytopenia (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 30,000/µL. Immediate platelet transfusion is recommended for patients experiencing severe bleeding, eg, intracranial or GI bleeding, and having a platelet count of <10,000/μL. In addition to platelet transfusion, specific therapies for ITP, including intravenous immune globulin, glucocorticoids, rituximab 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, recombinant von Willebrand factor, and von Willebrand factor/factor VIII 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 treatment of DIC is focused on addressing the underlying cause and managing the associated bleeding and thrombotic complications. The primary step is treating the underlying condition, eg, infection, trauma, malignancy, or obstetric complications. Supportive care is essential and may involve transfusion of FFP to replace depleted clotting factors, and platelet transfusions to correct thrombocytopenia. In cases of severe bleeding or organ failure, cryoprecipitate may be used to replenish fibrinogen. For thrombotic manifestations, heparin may be administered cautiously in selected cases, especially in the presence of microthrombi and organ ischemia. Antifibrinolytic agents (eg, tranexamic acid) are contraindicated in DIC due to the risk of exacerbating bleeding.

Differential Diagnosis

The following conditions should be considered when evaluating patients presenting with acute anemia:

• Trauma or hemorrhage

• GI bleed
  • Nonsteroidal anti-inflammatory drug (NSAID) or corticosteroid use
  • Alcohol use
  • Cirrhosis
  • Anticoagulant use

• Rupture of vascular aneurysm 
  • Particularly in areas like the aorta (aortic aneurysm) or cerebral vessels (intracranial aneurysm)
  • May present with sudden-onset tearing pain or loss of consciousness

• Surgery
  • Recent surgery involving moderate blood loss
  • History of bleeding disorders or excessive bruising
  • Use of antibiotics

• Heavy menstrual bleeding (excessive menstrual bleeding lasting >7 days)

• Nutritional deficiencies/malnutrition (eg, iron, vitamin B12, or folate deficiency) 

• Myelodysplastic syndrome (macrocytic anemia with leukopenia, macro-ovalocytes, and multi-lineage 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 (presents with weight loss, malaise, fevers, fatigue)

• Drug toxicity
  • Known or suspected ingestion of causative drug before the onset

• Pregnancy
  • Acute anemia in pregnancy is commonly caused by excessive blood loss during labor and delivery or exacerbated by nutritional deficiencies like iron or folate.
  • Leads to adverse outcomes such as preterm labor, low birth weight, and increased maternal morbidity.

Prognosis

The prognosis of acute anemia correlates with its severity, rate of development, and concurrent illnesses.[20][21][22][23][24] Severe acute anemia often worsens a patient's overall clinical status, imposing additional strain on the body and potentially accelerating the progression of underlying conditions. Prompt recognition and treatment of acute anemia are crucial, as delays in addressing the underlying cause can lead to significant complications and a rapid decline in the patient's health. 

Complications

The most severe complications of acute anemia arise from hypovolemic shock caused by significant hemorrhage. Reduced blood volume can lead to tissue hypoxia, precipitating end-organ damage including cardiac arrest, heart failure, renal failure, acute hypoxic respiratory failure, or other manifestations of organ dysfunction. Anemia has been known to compound acute ischemic stroke and atherosclerotic cardiovascular disease in general.[25] The presence of anemia correlates with an increased risk of heart failure and an overall poor prognosis (mortality and morbidity).[26] The patient's quality of life is generally impaired, and their (re)hospitalization rates are increased. Iron deficiency and erythropoietin insufficiency are the most common causative factors.