Causes of anemia

  • Decreased production of RBCs (Fe deficiency, kidney disease, cancer, EPO deficiency)
  • Blood loss (GI bleed, surgery)
  • Excessive destruction of RBCs (sickle cell anemia, autoimmune hemolytic anemia)
  • Normocytic anemia:  caused by chronic disease or blood loss
  • Microcytic anemia:  caused by Fe deficiency
  • Macrocytic anemia:  caused by either Folic acid or B12 deficiency
  • Normochromic anemia:  caused by acute loss of RBCs or aplastic anemia
  • Hypochromic anemia:  caused by severe Fe deficiency
  • Hyperchromic anemia:  caused by pernicious anemia
    • The amount of Hgb is what determines the intensity of the cell color
  • EPO initiates RBC production.  RBCs lifespan is shortened from its normal 120 day life cycle in pts with anemia.  Hepcidin regulates Fe absorption, recycling & mobilization from liver stores.
    • EPO levels will be higher in pts with anemia

Lab evaluation needed for anemia diagnosis

  • CBC including RBC indices
  • Reticulocyte index  (Low–indicates impaired RBC production with anemia;  High–indicates hemolysis or acute blood loss with anemia)
  • Mean corpuscular volume (MCV) = Hct/RBC.
    • MCV is the average volume of RBCs
    • FA & Vitamin B12 deficiencies will increase MCV
    • Iron Deficiency Anemia (IDA) will decrease MCV
  • Mean Corpuscular Hemoglobin = Hgb/RBC
    • It’s the % volume of Hgb in a RBC
    • FA & Vitamin B12 deficiencies will increase MCV
    • Iron Deficiency Anemia (IDA) will decrease MCV
  • Mean Corpuscular Hgb concentration = Hgb/Hct
    • It’s the weight of Hgb per volume of cells
    • Iron Deficiency Anemia (IDA) will decrease MCV
  • Heme stool test may also be used in the initial evaluation
  • Red cell distribution width (RDW)–the higher the more variable the RBC sizes
  • Serum Fe can fluctuate day to day
  • Total iron binding capacity (TIBC)
    • Low = malignancy
    • High = Fe deficiency anemia
  • % transferrin saturation = (serum Fe/TIBC) x 100        indicates the number of Fe binding sites that are vacant
  • Serum ferritin & folic acid levels
  • Vitamin B12 may be artificially low in folic acid deficiency
  • Homocysteine may be increased in folic acid or vitamin B12 deficiency
  • Methylmaolic acid (MMA) is increased only in Vitamin B12 deficiency
  • Coombs test:  if positive it indicates hemolytic anemia

Treatment for iron-deficiency anemia

  • Dietary supplementation, PO or IV Fe
    • Heme Fe (much more absorbable than non-heme Fe):  fish, meat, poultry
    • Non-heme Fe:  veggies, fruits, beans, nuts, grains
    • Want to increase vitamin C & meat intake while limiting milk & tea intake (avoid caffeine)
    • Want to give 200 mg of elemental Fe daily in 2-3 divided doses (FeSO4 300 mg TID)
      • Best to admin on an empty stomach if possible  (n/v/d/constipation & darkened stools are common SE)
      • Therapy should continue 3-6 months after the anemia has been resolved & reticulocytes & Hgb should be monitored
      • If the patient fails to respond due to non-compliance (misdiagnosis, malabsorption, or continued bleeding) you may need to proceed to IV Fe therapy
        • Need to monitor serrum ferritin, transferrin saturation & serum Fe levels monthly & Hgb/Hct levels weekly in patients on IV Fe therapy
    • Antacids, tetracyclines, caffeine, PPIs & H2 antagonists decrease the absorption of Fe
    • Fe decreases the absorption of fluoroquinolones, tetracyclines, levothyroxine, levodopa
  • In kids:  Drink  < 24 oz of milk/day, vitamin C can increase absorption
  • Prego:
    • Fe supplementation:  30 mg/day
    • Encourage eating Fe-rich food
  • Men & post-menopausal women require about 8 mg/day
  • Menstruating women (require 16 mg/day), kids & pregos require more Fe
    • Infants, kids, little girls, pregos & the elderly are at higher risk for developing iron deficiency anemia
      • In kids this may cause developmental delays, behavioral problems, increased absorption of lead
      • In pregos, IDA is associated with low birth weight, perinatal mortality.  Severe anemia can cause abnormal oxygenation, fetal cerebral vasodilation, death

Differences between folic acid and vitamin B12 deficiency anemia

  • Anemia:         men–  Hgb < 13 g/dL                  women– Hgb < 12 g/dL
  • Both are megaloblastic anemias
  • Vitamin B12 deficiency anemia:
    • More common in women, incidence increases with age
    • Caused by
      • inadequate intake  (seen in vegans, chronic alcoholics, elderly who don’t get enough intake of meats, dairy, etc)
      • decreased absorption (pernicious anemia–due to a lack of intrinsic factor as confirmed by Schilling’s test or cobalamin malabsorption–inability to cleave vitamin B12 from foods, caused by inadequate gastric acid production)
      • inadequate utilization
    • S/S:  neuropsychiatric symptoms–may be irreversible (irritability, dementia, memory changes, ataxia, muscle weakness, peripheral neuropathies)
    • Antibiotics, anticonvulsants, cytotoxic agents, oral contraceptives & high dose vitamin C can cause falsely low levels
    • MMA levels are high in vitamin B12 anemia
    • Treatment:  dietary counseling, oral vitamin B12 (1 mg/day) –> if oral doesn’t work, switch to IV or IM
      • SE:  hyperuricemia, hypokalemia, potential for thrombosis, fluid retention, anaphylaxis
  • Folic acid deficiency anemia
    • Can be caused by excessive alcohol intake or pregnancy
    • Dietary sources of folic acid:  green leafy veggies, fruits, yeast, mushrooms, liver, kidney
    • Causes:
      • Inadequate intake (elderly, alcoholics, teens, poor ppl, chronically ill)
      • Decreased absorption (bactrim, 5-FU, methotrexate, malabsorption syndromes, alcohol)
      • Hyperutilization (prego, growth spurts, cancer, LT dialysis, hemolytic anemia, Crohn’s disease, rheumatoid arthritis)
      • Inadequate utilization (alcohol)
    • S/S:  similar to vitamin B12 deficiency but there aren’t any neurological symptoms
    • Labs are similar to vitamin B12 anemia but B12 levels are normal & MMA levels are normal, decreased folate levels
    • Treatment:  Folic acid 1 mg daily (may need up to 5 mg/d for malabsorption) continue for 4 months unless chronic disease.  Maintain a diet rich in folic acid.

Treatment of choice, including doses, for anemia of chronic disease

  • Occurs in diseases lasting longer than 1-2 months (chronic infections, chronic inflammation, malignancies, HF)
    • Diagnosis is generally made by ruling out other causes, Fe is ineffective during inflammation
  • Decreased lifespan of RBCs, decreased response of EPO, disturbance of Fe metabolism, impaired proliferation of EPO cells
  • Treatment:
    • Treat underlying cause
    • Transfusions:  limit to inadequate oxygen transportation
    • EPO alpha–especially for patients with compromised CV status
    • Epoetin (Procrit) 50-100 u/kg SQ 3x/week     or     10,000 u SQ q week
      • SE:  HTN, seizures, diarrhea
    • Darbepoetin alpha (aranesp) has a longer half-life than EPO
      • 0.45 mcg/kg q week        SQ or IV
      • 0.75 mcg/kg q 2 weeks
      • SE:  HTN, hypotension, edema, n/v, abdominal pain, myalgias
    • Supplemental Fe may be needed if % transferrin saturation < 20 %  & serum ferritin < 100 ng/mL
      • Most hemodialysis patients require IV Fe
      • Need to admin 100-125 mg of Fe with each dialysis session for 8-10 weeks
      • Once these goals are reached, give Fe weekly
    • If transferrin sat > 50% & serum ferritin > 800 ng/mL, stop Fe therapy for up to 3 months & recheck Fe parameters before restarting (but once you do restart, do it at half to a third the dose)
    • Monitor:
      • Hgb q 1-2 weeks during initiation & then q 2-4 weeks once stable  (goal is Hgb = 11-12 mg/dL)
      • Serum Fe initially & periodically
      • If no response by 8 weeks, then d/c therapy

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