• Anemia is defined as a hemoglobin concentration <12 g/dL in females and <13 g/dL in males.
• Red blood cells (RBCs) with normal functioning hemoglobin (Hg) are essential for delivering oxygen to tissues. They also contribute to blood viscosity and may aid in hemostasis.

• Decreased or impaired production
  • Nutritional deficiencies (iron, folate, vitamin B12)
  • Reduced erythropoietin (EPO) production due to renal failure
  • Bone marrow causes: Aplastic anemia, dysplasia/cancer, or fibrosis
  • Chronic inflammation (also known as anemia of chronic disease [ACD])
• Increased destruction (hemolysis)
  • Intrinsic to RBCs
    • Membrane disorders
    • Hemoglobinopathies: Sickle cell disease, thalassemia
    • Enzyme deficiencies
  • Extrinsic to RBCs
    • Immune (allo or autoantibody mediated)
    • Microangiopathy (disseminated intravascular coagulation, thrombotic thrombocytopenic purpura)
    • Macroangiopathy (leaky valve)
  • Infections (malaria)
    • Other (burns)
• RBC loss
  • Bleeding (GI bleeding, menorrhagia, surgery, etc.)
  • Blood donation
• RBC sequestration (related to splenomegaly)
• Dilution
  • Iatrogenic (e.g., resuscitation with crystalloid)
  • Pregnancy

• The mechanisms of anemia-induced morbidity and mortality have not been clearly established. However, inadequate blood oxygen content and tissue oxygen delivery likely contribute (2,7).
• Iron deficiency can result from poor nutritional intake, increased requirements (childhood, pregnancy, breastfeeding), chronic blood loss, and impaired absorption (1).
• Vitamin deficiency can result from poor oral intake, impaired absorption or increased requirements (e.g., folate deficiency in hemolysis).
• Renal failure leads to impaired EPO production which in turn results in anemia.
• ACD is a result of chronic inflammation. Pro-inflammatory mediators and RES cells induce changes in iron homeostasis, proliferation of erythroid progenitor cells, production of EPO, as well as affect the life span of red cells leading to anemia.
• Hemolytic anemia is a result of impaired red cell survival due to a variety of factors, and can be either hereditary or acquired.
• Malignancy, both hematological and solid, may lead to anemia due to tumor occupying the bone marrow, or bone marrow suppression resulting from the treatment of malignancy (irradiation, chemotherapy) or from ACD.
• In addition to iron deficiency, pregnancy leads to increased plasma volume and dilutional anemia. Dilutional anemia may also result from aggressive crystalloid resuscitation of patients who present with bleeding.

• Each unit of transfused RBCs increases the Hg level by ~1 g/dL and Hct by 3%.
• The decision to transfuse should not be based solely on Hg level; the clinical situation must be taken into account. Most guidelines recommend transfusion for a euvolemic Hg <6.5 g/dL. Transfusion is almost never indicated for a euvolemic Hg level >10 g/dL. The area between 6.5 and 10 dg/L is a gray zone, and the decision to transfuse should depend upon clinical circumstances including ongoing blood loss, presence of relevant comorbidities, symptoms of anemia, and signs indicative of inadequate oxygen delivery or hemodynamic instability.

• Fatigue, lightheadedness, syncope, impaired mentation
• Palpitations
• Shortness of breath and/or chest pain on exertion
• Jaundice, dark urine, gallstones (suggestive of hemolytic anemia)

Iron, erythropoiesis-stimulating agents (ESA), Vitamin B12, folate, transfusions

Medications with myelotoxic potential: Immunosuppressive agents (e.g., Imuran), chemotherapy (e.g., cyclophosphamide), anticonvulsants, etc.

Concomitant lung or heart disease may lower the body's ability to compensate for anemia. These patients may have symptoms of anemia at higher Hg levels than their healthy peers.

• Symptoms of impaired oxygen delivery to the cerebral or myocardial system
• If significant anemia (Hg <10 g/L) is present and surgery could be safely postponed, a patient should undergo evaluation by an internist or hematologist and treated for anemia prior to surgery. This is especially true for patients who will be undergoing high blood loss procedures, have a rare blood type, or significant alloimmunization against RBC antigens, or those who object to blood transfusion for religious reasons.

• Morphological: Microcytic, macrocytic, normocytic
• Kinetic: Decreased RBC production, increased RBC destruction, increased RBC loss, sequestration and dilution

Not applicable

• Follow Hg levels closely, as well as symptoms and bleeding; consider transfusion as appropriate. Over-transfusion should be avoided; in stable patients, transfuse 1 unit at a time followed by reassessment.
• Eliminate unnecessary blood draws; collect samples into pediatric tubes.
• Consider consulting hematology or the blood conservation service to assist with iron supplementation and other medical therapy for optimization of Hg.
• Do not forget about appropriate thromboprophylaxis especially for those patients who have received ESA and tranexamic acid (TXA) perioperatively.

• Blood Oxygen Carrying Capacity
• Mixed Venous Oxygen Saturation
• Transfusion Related Lung Injury (TRALI)
• Transfusion Infections

• 280.9 Iron deficiency anemia, unspecified
• 284.9 Aplastic anemia, unspecified
• 285.9 Anemia, unspecified
• 285.1 Acute posthemorrhagic anemia
• 280.0 Iron deficiency anemia secondary to blood loss (chronic)

• D50.9 Iron deficiency anemia, unspecified
• D61.9 Aplastic anemia, unspecified
• D64.9 Anemia, unspecified
• D62 Acute posthemorrhagic anemia
• D50.0 Iron deficiency anemia secondary to blood loss (chronic)

Gregory M. T. Hare , MD, PhD

Katerina Pavenski , MD, FRCPC