Anemia is a common issue encountered in the family medicine. By definition it is a deficit of red blood cells or hemoglobin. It is important to identify the underlying etiology to further manage this issue.

History Edit

  • fatigue, weakness, dyspnea, CP, palpitations, decreased exercise tolerance, pre-syncope, syncope
  • Symptoms of infection/recurrent, malignancy, blood loss, ongoing bleeding
  • PMHx: mechanical valves
  • Medications: anticoagulants, anti-platelets, new medications
  • SHx: Diet, ETOH

Physical Edit

  • Vitals + volume status (red flags, tachycardia/hypotension/fluctuation in LOC)
  • Skin/LN: angular chelosis,pallor, jaundice, lymphadenopathy, petechiae, glossitis, nail changes (brittle)
  • Chest: orthostatic hypotension, systolic flow murmur, wide pulse pressure, signs of CHF
  • Abdo: HSM, masses, DRE
  • Neuro: proprioception (if suspecting B12 deficiency)

Approach to Anemia Edit

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Microcytic AnemiaEdit


  • T - thalassemia
  • A- Anemia of chronic disease
  • I - Iron deficiency anemia (IDA)
  • L- Lead poisoning
  • S - Sideroblastic anemia


  • CBC (microcytic anemia, RDW), Ferritin, TIBC, serum iron 
  • +/- lead level, HbG electrophoresis, blood smear
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Iron deficiencyEdit

  • Etiology:
    • increase demand (e.g. pregnancy, lactation, growing child)
    • decrease supply (diet, malabsorption)
    • increase loses (hemorrhage, intravascular hemolysis)
  • Screening: immigrants, refugees, pregnancy
    • high risk pediatric patients (well baby care): preterm or low birth weight, infants introduced to cows milk < 12 months of age, breast fed infants without adeqate iron in diet after 6 months, children who consume >24 oz daily of cow's milk, special health concerns (chronic disease, trauma, surgery, medications, diets), 
    • also consider screening: children in poverty, poor weight gain, or poor diet
  • Work-up:
    • Attempt to identify a source of bleeding
    • Initial investigation of microcytic anemia --> ferritin 
    • If male of any age or non-menstuating female --> Evaluate for GI source (endoscopy/colonoscopy)
    • If neither male/non-menstruating female a trial of iron is acceptable x 1 month (should see increase in HbG by 10-20). If not evaluate for GI source/malabsorption. If see improvement continue iron x3-6 months to be replenish stores then r/a
    • In anemic patients with menorrhagia, determine the need to look for other causes of the anemia
  • Treatment:
    • If clinical status is compromised by moderate to severe anemia consider admission to acute care facility and blood transfusion
    • Prevention: encourage full balanced diet
    • Oral preparations preferred over IV form
    • Oral: Target 100mg of elemental iron 3x/day
    • Best absorption on empty stomach with addition of Vitamin C. Absorption may be decreased by antacids, supplemetation (aluminum, magnesium, zinc, calcium). Recommend 2 hours between taking Rx.
    • Iron can decrease absorption of bisphosphonate, tetracycline, fluroquinolones, levodopa, thyroid rx
    • S/E: nausea, vomit, dyspepsia, constipation dark stool, bloating (can trial smaller dose)
    • After HbG returns to normal should be continued for 3-6 months to restore iron stores

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Anemia of Chronic Disease

  • Etiology: underproduction and impaired iron utilization
  • Diagnosis: of exclusion, often co-exists with iron deficiency
  • Treatment: manage underlying, may consider transfusion/erythropoietin PRN

Lead PoisoningEdit

  • LEAD: lead lines (epiphysis of long bones, gingivae), encephalopathy, abdominal pain colicky/anemia (basophilic stippling), Drops (wrist, foot)
  • Diagnosis: lead level
  • Treatment: remove source, chelation therapy, EDTA (adults)

Sideroblastic AnemiaEdit

  • Etiology: defect in heme biosynthesis in RBC precursors (hereditary x-linked, reversible, and idiopathic forms)
  • Diagnosis: smear (ringed sideroblasts), bone marrow biopsy
  • Treatment: heriditary (high dose B6), acquired (Epo and G-CSF), reversible (remove precipitating)


  • Etiology: defect in production of alpha or beta chains of HbG (4alpha, 2 beta)
  • Beta-thalassemia: common in Mediterranean, Asian
  • Alpha- thalassemia: Asians and Africans
  • Diagnosis: HbG electrophoresis

Normocytic AnemiaEdit

High reticulocytesEdit

  • Blood loss - reticulocyte count can be normal at initial onset of bleeding
  • Hemolysis - peripheral smear, LDH (increased), haptoglobin (decreased), indirect bilirubin (increased)
    • Inherited:
      • Hemoglobinopathies - thalassemia, sickle cell. W/U HbG electrophoresis
      • Abnormal membrane (hereditary spherocytosis) - W/U: osmotic fragility test. Rx: vaccinations, splenectomy
      • Abnormal enzymes (G6PDeficiency, pyruvate kinase deficiency)- W/U: enzyme assays
    • Acquired
      • Autoimmune (cold/warm) W/U: direct Coomb's testing 
      • Infection (e.g. malaria)
      • Microangiopathic hemolytic anemia (MAHA) (intravascular hemolytic anemia)
        • TTP, DIC, HEELP, malignant hypertension, vasculitis
        • W/U: peripheral smear (schistocytes), hemolytic w/u, urine hemoglobinuria
      • Drug related

Low reticulocytesEdit

  • Pancytopenia: aplastic anemia, MDS, myelofibrosis, leukemia, TB, amyloidosis, sarcoidosis, drugs
    • Investigation: bone marrow aspiration
  • Non-pancytopenia: anemia of chronic disease, liver disease, renal disease

Sickle Cell AnemiaEdit

  • Etiology: mutation B-globin chain Glu-->Val
  • Higher incidence in African and Mediterranean
  • Sickle cell disease = two HbS (HbSS) - sickling occurs at pO2 80mmHg. Sickle cell trait HbAS - sickling occurs at pO2 40mmHg
  • Clinical: hemolytic anemia, jaundice, growth retardation, spenomegaly (functional asplenism), aplastic crisis, splenic sequestration crisis, vaso-occlusive crisis (pain, chest), priapism
  • Diagnosis: Peripheral smear, HbG electrophoresis
  • Treatment:
    • folic acid
    • Hydroxyurea (promotes HbF (fetal))
    • Manage vaso-occlusive events: hydration, analgesics, Abx, magnesium, exchange transfusion
    • Avoid conditions that promote sickling (acidosis, hypoxia, dehyration, fever)
    • Vaccination

Macrocytic AnemiaEdit

  • Megaloblastic: B12 deficiency, folate deficiency, drug related (e.g. MTX)
  • Non-megaloblastic: alcohol, hypothyroidism, MDS, liver disease, reticulocytosis
  • Investigations can include: b12 level, folate level, TSH, peripheral smear, LFTs, reticulocyte count, +/- bone marrow aspiration
  • B12 deficiency: confusion, ataxia, symmetric peripheral neuropathy (propioception/vibration - dorsal columns), memory loss, dementia, personality changes
    • Etiology:  pernicious anemia (antibodies to intrinsic factor), diet (vegetarian), post-gastrectomy, intestinal malabsorption (crohn's, celeiac, tapeworm, drugs, pancreatic insufficiency)
      • If intestinal absorption okay --> 1200mcg PO daily
      • If intestinal absorption impaired (e.g. pernicious anemia - lacking intrinsic factor)--> Intramuscular
      • Investion for pernicious anemia versus other causes use to be schilling test 

Special Population and ConsiderationsEdit

Iron deficiency in pediatricsEdit

  • risk of irreversible motor and cognitive deficits
  • Introduce iron rich food at 6 months
  • Treatment: look for source, ferrous sulphate 3-6mg of elemental iron/kg/day in divided dosing. Monitor for toxicity

Iron deficiency in PregnancyEdit

  • Recommend increase in iron consumption by 15-30mg elemental iron/day for pregnancy/breastfeeding in non-anemic women
  • Anemia is pregnancy T1 HbG < 110, T2 HbG < 104, T3 HbG < 110

Anemia in elderlyEdit

  • Often multifactorial
  • Recommend investigations if > 1 year of life or symptomatic


  • If symptomatic - transfuse
  • Cut-off (these are general cut-offs)
    • stable but critically ill with no active bleed --> Transfuse HbG < 70
    • patientw with ischemic heart disease wtth no active bleed --> Transfuse HbG 90-100

Peripheral Blood SmearEdit

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uptodate- anemia

dietary aspects of iron

Toronto Notes 2012