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Iron Deficiency Anemia
Prevalence
NFHS-3 : 7/10 children aged 6-59 months are
anemic. (3%-severely anemic, 40%-moderate
anemic, 26%- mildly anemic)
65% in preschool children
Adolescent period -50%
Iron deficiency affects 2170 million
worldwide, and 1200 million of them anemic with
90% of affected are in developing countries
Total Body Iron
Full-term infants - approximately 75 mg/kg
body weight of iron
Adult males – 50 mg/kg and females – 35
mg/kg
Can be divided into functional(80%) and
storage(20%) compartments
Iron Balance
Mostly lost from shedding of epithelial cells in
G.I.Tract.
Total average daily loss of iron has been
estimated at ∼1.0 mg in normal adult men and
nonmenstruating women.
20% of heme iron (in contrast to 1% to 2% of
nonheme iron) is absorbable.
Iron balance is primarily, if not
exclusively, achieved by control
of absorption rather than by
control of excretion
The “Iron cycle”
Since plasma ferritin is derived
largely from the storage pool of
body iron, its levels correlate well
with body iron stores.
Nutritional Iron Balance
Role of Hepcidin
Synthesized and released from the liver
Inhibits iron transfer from the enterocyte to
plasma
Regulator of iron absorption
Also suppresses iron release from
macrophages
Important role in anemia of chronic diseases
and hemochromatosis
Very high levels of hepcidin in
Anemia of chronic diseases and
inappropriately low levels of
hepcidin in hemochromatosis
Etiology
Late manifestation of prolonged negative
iron balance
As a result of major blood loss
Increased physiologic need for iron
Diet
Body iron concentration in normal neonates averages
∼75 to 100 mg/kg weight
Premature infants are at higher risk of iron deficiency
Delayed cord clamping
The fetus is an “effective scavenger of maternal iron”
Normal term infant must acquire 135 to 200 mg of iron
during the first year of life. A premature infant may
require as much as 350 mg in the same period
 Iron stores in the infant are typically depleted by 4 to
6 months of age
 Iron intake of 1 mg/kg/day is recommended for full-
term infants, 2 to 4 mg/kg/day for preterm infants
 Deficiency is relatively uncommon in the first 6
months of life in infants exclusively fed breast milk
 Cow’s milk should not be given to infants <1 year of
age
Blood loss
• Lesions of the gastrointestinal (GI) tract - peptic
ulcer, Meckel diverticulum, polyp, hemangioma, or
inflammatory bowel disease
• Heat-labile protein in whole bovine milk
• Chronic diarrhea and rarely with pulmonary
hemosiderosis
• Parasitic infestations and H.pylori infection
Clinical Features
Pallor, anorexia and irritability
Hyperdynamic circulation
Skin and nail changes
Pica - 70-80% of Children
Koilonychia
Consequences of Iron Deficiency
Long term mental impairment
Impaired immune function
Poor physical performance
Febrile seizures, temper tantrums, breath
holding spells, restless leg syndrome.
Lab evaluation
Hemoglobin, Hematocrit
Red cell indices
Reticulocyte hemoglobin content (CHr)
Mentzer index and RDW
Serum ferritin
Serum iron, TIBC, Transferrin saturation
Stainable iron in bone marrow
Stool for occult blood
Treatment
 Depends on severity and associated complications
 3-6 mg/kg of elemental iron in 3 divided doses is
adequate
 Ferrous sulfate is 20% elemental iron by weight
and is ideally given between meals with juice
 Addition of folic acid and vitamin C (200
mg), vitamin B12.
Parenteral Iron
 Should usually be avoided
 Severe side effects on oral therapy, noncompliance or
gastrointestinal bleeding
 Total dose infusion (only in hospital)
 Iron dextran or sucrose complex - most commonly used
 Iron required=wt (kg)x 2.3x (15-patient hemoglobin)
+500-1000 mg
Response to Iron therapy
TIME AFTER IRON ADMINISTRATION RESPONSE
12-24 hr
Replacement of intracellular iron
enzymes; subjective improvement;
decreased irritability; increased
appetite
36-48 hr
Initial bone marrow response;
erythroid hyperplasia
48-72 hr Reticulocytosis, peaking at 5-7 days
4-30 days Increase in hemoglobin level
1-3 months Repletion of stores
Nonresponders to Iron therapy
 Incorrect dose or medication
 Malabsorption of administered iron
 Ongoing blood loss including gastrointestinal, menstrual, and pulmonary
 Concurrent infection or inflammatory disorder inhibiting the response to
iron
 Concurrent vitamin B12 or folate deficiency
 Diagnosis other than iron deficiency
 • Thalassemias
 • Anemia of chronic disease
 • Lead poisoning
 • Sickle thalassemias, hemoglobin SC disease
 • Rare microcytic anemias
Prevention
• Medicinal iron supplementation
• Dietary modification
Balance between inhibitors and promoters
Vitamin C rich foods
Fermentation and germination
• Food fortification
Double fortified salt
Weekly Iron and Folic acid
Supplementation (WIFS)
Iron deficiency anemia
Iron deficiency anemia
Iron deficiency anemia

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Iron deficiency anemia

  • 2. Prevalence NFHS-3 : 7/10 children aged 6-59 months are anemic. (3%-severely anemic, 40%-moderate anemic, 26%- mildly anemic) 65% in preschool children Adolescent period -50% Iron deficiency affects 2170 million worldwide, and 1200 million of them anemic with 90% of affected are in developing countries
  • 3. Total Body Iron Full-term infants - approximately 75 mg/kg body weight of iron Adult males – 50 mg/kg and females – 35 mg/kg Can be divided into functional(80%) and storage(20%) compartments
  • 4. Iron Balance Mostly lost from shedding of epithelial cells in G.I.Tract. Total average daily loss of iron has been estimated at ∼1.0 mg in normal adult men and nonmenstruating women. 20% of heme iron (in contrast to 1% to 2% of nonheme iron) is absorbable.
  • 5. Iron balance is primarily, if not exclusively, achieved by control of absorption rather than by control of excretion
  • 7. Since plasma ferritin is derived largely from the storage pool of body iron, its levels correlate well with body iron stores.
  • 9. Role of Hepcidin Synthesized and released from the liver Inhibits iron transfer from the enterocyte to plasma Regulator of iron absorption Also suppresses iron release from macrophages Important role in anemia of chronic diseases and hemochromatosis
  • 10. Very high levels of hepcidin in Anemia of chronic diseases and inappropriately low levels of hepcidin in hemochromatosis
  • 11. Etiology Late manifestation of prolonged negative iron balance As a result of major blood loss Increased physiologic need for iron
  • 12. Diet Body iron concentration in normal neonates averages ∼75 to 100 mg/kg weight Premature infants are at higher risk of iron deficiency Delayed cord clamping The fetus is an “effective scavenger of maternal iron” Normal term infant must acquire 135 to 200 mg of iron during the first year of life. A premature infant may require as much as 350 mg in the same period
  • 13.  Iron stores in the infant are typically depleted by 4 to 6 months of age  Iron intake of 1 mg/kg/day is recommended for full- term infants, 2 to 4 mg/kg/day for preterm infants  Deficiency is relatively uncommon in the first 6 months of life in infants exclusively fed breast milk  Cow’s milk should not be given to infants <1 year of age
  • 14. Blood loss • Lesions of the gastrointestinal (GI) tract - peptic ulcer, Meckel diverticulum, polyp, hemangioma, or inflammatory bowel disease • Heat-labile protein in whole bovine milk • Chronic diarrhea and rarely with pulmonary hemosiderosis • Parasitic infestations and H.pylori infection
  • 15.
  • 16. Clinical Features Pallor, anorexia and irritability Hyperdynamic circulation Skin and nail changes Pica - 70-80% of Children
  • 18.
  • 19.
  • 20. Consequences of Iron Deficiency Long term mental impairment Impaired immune function Poor physical performance Febrile seizures, temper tantrums, breath holding spells, restless leg syndrome.
  • 21.
  • 22. Lab evaluation Hemoglobin, Hematocrit Red cell indices Reticulocyte hemoglobin content (CHr) Mentzer index and RDW Serum ferritin Serum iron, TIBC, Transferrin saturation Stainable iron in bone marrow Stool for occult blood
  • 23.
  • 24.
  • 25. Treatment  Depends on severity and associated complications  3-6 mg/kg of elemental iron in 3 divided doses is adequate  Ferrous sulfate is 20% elemental iron by weight and is ideally given between meals with juice  Addition of folic acid and vitamin C (200 mg), vitamin B12.
  • 26. Parenteral Iron  Should usually be avoided  Severe side effects on oral therapy, noncompliance or gastrointestinal bleeding  Total dose infusion (only in hospital)  Iron dextran or sucrose complex - most commonly used  Iron required=wt (kg)x 2.3x (15-patient hemoglobin) +500-1000 mg
  • 27. Response to Iron therapy TIME AFTER IRON ADMINISTRATION RESPONSE 12-24 hr Replacement of intracellular iron enzymes; subjective improvement; decreased irritability; increased appetite 36-48 hr Initial bone marrow response; erythroid hyperplasia 48-72 hr Reticulocytosis, peaking at 5-7 days 4-30 days Increase in hemoglobin level 1-3 months Repletion of stores
  • 28. Nonresponders to Iron therapy  Incorrect dose or medication  Malabsorption of administered iron  Ongoing blood loss including gastrointestinal, menstrual, and pulmonary  Concurrent infection or inflammatory disorder inhibiting the response to iron  Concurrent vitamin B12 or folate deficiency  Diagnosis other than iron deficiency  • Thalassemias  • Anemia of chronic disease  • Lead poisoning  • Sickle thalassemias, hemoglobin SC disease  • Rare microcytic anemias
  • 29. Prevention • Medicinal iron supplementation • Dietary modification Balance between inhibitors and promoters Vitamin C rich foods Fermentation and germination • Food fortification Double fortified salt
  • 30. Weekly Iron and Folic acid Supplementation (WIFS)

Notas del editor

  1. As much as 100 ml of fetal blood may remain in the placenta with early clamping of the cord. Cord clamping delayed for only 3 minutes can result in a 58% increase in red cell volume.a similar effect can be achieved by clamping the cord at the placental end, raising the clamp, and allowing gravity to drain the cord depletion of maternal iron has little or no effect on the body iron stores of the newborniron supplementation during pregnancy has no effect on the subsequent development of iron deficiency in the infant, although it may be protective for the mother
  2. A unique disorder termed Bahima disease, described in Uganda, was attributed to the practice of feeding children a diet of cow’s milk almost exclusively