Iron-deficiency anemia
also see Anemia, General Approach
Iron in the body:
- 65% in hemoglobin (in the
red blood cells)
- 30% stored as ferritin in
the liver, bone marrow, and spleen.
- 4% in myoglobin (in
skeletal muscle)
- A small percentage is in transport, as part of
transferrin, traveling between
various parts of the body via the blood stream.
Labs
- iron deficiency usually does not cause a
microcytic anemia until the hematocrit drops below 30%.
- Ferritin is useful for diagnosing iron
deficiency. Since ferritin is an acute phase reactant, some say it should not
be used in the setting of inflammation; others say that in chronic
inflammation a ferritin < 50 is highly suggestive of iron deficiency.
- Mentzer Index
- RDW (reflecting anisocytosis) is high.
- Serum iron, transferrin and TIBC
- A serum iron test actually
measures the amount of iron in
transferrin.
- Each transferrin molecule can carry 2 iron atoms, and normally, about
30% of the available "spaces" for iron are filled. By artificially filling
up all the available spaces, doctors can measure the total iron binding
capacity, or TIBC, of your blood.
Think of transferrin as a gang of
motorcycles. TIBC
relates to the number of empty seats in the motorcycle gang. TIBC is
usually higher-than-normal when the body's iron stores are low; there are
empty motorcycles, because there are fewer potential passengers in the
neighbourhood.
- Normal Values: iron: 60-170 mcg/dl, TIBC: 240-450 mcg/dl, transferrin
saturation: 20-50%
- Higher-than-normal TIBC may indicate: iron deficiency anemia, pregnancy
(late)
- Lower-than-normal TIBC may indicate: cirrhosis, hemolytic anemia,
hypoproteinemia, pernicious anemia, sickle cell anemia, inflammation,
malnutrition, liver disease
Iron deficiency: signs and symptoms: decreased work capacity, growth
retardation, increased susceptibility to infection, irritability, stomatitis,
glossitis, cheilitis, disaccharidase deficiency, increased lead absorption,
craving for ice (pagophagia), lower IQ scores/decreased scholastic performance
Iron-Deficiency anemia associated with excessive milk intake
There are 5 reasons that increased milk ingestion causes iron deficiency:
- When children ingest large amounts of milk, they do so
at the expense of other iron-rich
foods. Therefore, iron intake is inadequate.
- Milk irritates the GI
lining, leading to small microhemorrhages. Therefore, GI blood loss.
- These factors decrease iron absorption:
- Calcium
- fat
in milk
- milk
neutralizes stomach acid. Increased pH inhibits Fe absorption to some
degree.
Treatment consists of limiting milk ingestion to 16-20 oz of milk/day and
supplementing with Fe 6 mg/kg/day. Recheck hemoglobin in 1 month. If it's pure
iron deficiency anemia, the hemoglobin should be back up to normal, and then
continue the Fe therapy for 4-6 more months. If the hemoglobin is still low,
you need to check a full CBC, looking for other causes of a microcytic anemia,
such as thalassemia.
Therapy
- Ferrous iron 4-6 mg/kg /day div bid/tid. Also see
Iron Toxicity
- Give on empty stomach, with Vit-C containing juice to increase absorption
(lower pH aids absorption)
- Transfuse only if cardiovascular compromise (rare)
- Parental iron dextran only for severe non-compliance, malabsorption, or if
ongoing loss exceeds absorption capacity
- Iron Containing Foods: meats, fish, poultry. Also raisins, dried fruit,
sweet potatoes, lima beans, chili beans, green peas, peanut butter, and
enriched foods
Follow-up
- Retic count should double in 1-2 weeks
- Hb should rise 1 g/dl in 2-4 weeks
- Check
CBC and
retic count at 2 weeks to assess response
- continue iron for 3
mos to replete body stores
Neonatal iron deficiency is very
uncommon because iron transport across the placenta is programmed to
support the fetus, even in the face of maternal iron deficiency. As neonatal
erythropoiesis declines markedly in the first 6 to 8 weeks after birth,
iron from red blood cell breakdown is
salvaged by the
reticuloendothelial system,
augmenting neonatal iron stores. As the infant emerges from the
physiologic nadir and active erythropoiesis resumes, adequate iron stores must
be present to support this process. In
term infants, iron stores rarely are depleted before 4 months of age, and
iron deficiency anemia is unlikely to occur if iron-fortified cereal or other
solid foods are introduced by 6 months of age.
In preterm infants, total body iron is less at birth than in term infants, and
neonatal iron stores are depleted more rapidly. Iron deficiency can, therefore,
develop by 2 to 3 months of age in preterm infants who are either breastfed or
bottle-fed with a formula that is not iron-supplemented. It is generally
recommended that preterm infants begin iron supplementation at 1 month of age,
either as iron-fortified formula or as iron supplementation in breastfed
infants. (PREP 2004)