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Nutritional Anemia
Dr. Narayana L
SR Paediatrics
Definition
• Reduction in oxygen carrying capacity of blood as a result
of decreased :
– Red cell mass
– Red Cell count / HCT
– Hb concentration
WHO cutoffs for Anemia
Age group Hemoglobin (Hb) Hematocrit (PCV)
6 Mo to 5 yr <11.0 <33
5 – 11 Yr <11.5 <34
11 – 13 Yr <12.0 <36
Non pregnant
women
<12.0 <36
Men <13.0 <39
Problem Burden
• Anemia is a global public health problem especially
in south east asia, africa and south america
• Nutritional anemia -major public health problem in
India
• 7 out of every 10 children aged 6-59 months are
anemic in India
Classification
• Aetiological
– ↓Production: e.g. aplastic anemia
– Hemolysis: e.g. G6PD deficiency
– Hemorrhage: e.g. rectal polyp
• Rate of onset
– Acute: e.g. malaria with hemolysis
– Chronic: e.g. Iron deficiency anemia
• Severity
– Mild 10 gm %
– Moderate 7-10 gm%
– Severe < 7 gm%
Nutritional Anemia
• Iron
• Folic acid
• Vit. B12
• Others: Protein, Zinc, Copper, Vit. C
• Deficiency of any of these will lead to a
chronic state of nutritional anemia
Approach To Any Anemia
• Detailed History
• Detailed head to toe examination
• Screening laboratory tests
• Confirmatory tests
Anemia - History
• Age / Sex / Inheritance
• Infections & Worms
• Drugs
• Diet, Pica
• Community
History in Nutritional anemia
• Symptoms of anemia: Fatigue, shortness of
breath, lassitude, weakness, Dyspnea on Exertion
• Age of onset: 6 mo-36 months
• Sex: Both sexes equally affected in childhood,
after adolescence females > males
• Diet: Lack of breast feeds, excess of milk based
diet, bottle fed, poor weaning food, predominantly
vegetarian diet, pure vegan (B12 def.)
History in Nutritional anemia – Contd..
• H/O Pica: Altered appetite for mud, chalk, pencil,
color, raw food items etc. – Both cause and effect
• H/O irritability, crankiness, stubbornness,
listlessness
• H/O breath holding spasms,
• Infections: Common as a cause of anemia, rule
out worms infestation esp. hook worm, round
worms, giardia,
Anemia – Physical Exam
• Signs of anemia: Pallor, Puffiness, Edema feet, hemic
murmer
• Tongue: Pallor, Bald & shining tongue, loss of papillae,
Angular cheilosis (IDA)
• Nails: Platynychia, Koilonychia (IDA)
Hyperpigmented knuckles (Megaloblastic anemia)
• Fidgety, irritable, cranky, listless child,
• Resents strangers and examination
Common Manifestations
Loss of Papillae Pale & Bald tongue
Platynychia Hyperpigmented knuckles
Anemia – Physical Exam – Contd..
• To rule out other causes of anemia look for:
• Abnormal facies (e.g. Hemolytic facies)
• Hepatosplenomegaly (e.g. Thalassemia)
• Lymphadenopathy (infections, TB, malignancies)
• Bony tenderness (e.g. leukemia)
• Petechiae/purpura (aplastic anemia, leukemia)
• Weight loss (malignancies)
• Skeletal changes (e.g. Fanconi’s anemia)
Laboratory Investigations
• Screening tests
– Hb, HCT
– Red cell indices
– Reticulocyte count
– P.S. examination
• Confirmatory tests
RDW values in various diseases
RDW Low MCV Normal MCV High MCV
Normal
Thalassemia
trait
Normal
Aplastic
anemia
High IDA
Chronic liver
disease,
malignancies,
myelofibrosis,
myelotoxic
drugs
Megalo. An.,
Imm. Hem.
An.
Reticulocyte Count
• Count 500 cells - supravital
staining
• Normal : 1-2%
• Low count: BM depression
like aplastic anemia, BM
infiltration, PRCA
• High count: Good BM
response like in hemolysis,
hemorrhage, post-treatment
Advantages of PS examination
• Bedside, easily available
• Cost effective, Imp. Info.
• Types of anemia
• At times diagnostic
• ↓need for further tests
PS examination
Normocytic Normochromic
Macrocytic – Megaloblastic anemia
Microcytic Hypochromic – IDA
Microcytic Hypochromic –
Thalassemia (Target cells, NRs)
Blood Film
Red cell Indices
Hypochromic
Microcytic
MCV < 80μ3
MCH < 29 ρg
MCHC < 32 %
Normocytic
Microcytic
MCV 75-95 μ3
Morphological Classification
Macrocytic
MCV > 95μ3
Microcytic, Hypochromic Anemia D.D.
MCV < 80μ3, MCH < 29 ρg., MCHC < 32%
• IDA
• Hemoglobinopathies
• Anemia of chronic infections
• Sideroblastic Anemia
• Lead poisoning
PS Exam. / Red Cell indices
Hypochromic Microcytic Anemia
MCV < 80u3, MCH < 20 Pg., MCHC < 32%
Normal / Decreased Normal / Increased
Sr. Iron
Iron Store, Sr. Ferritin Abnormal Normal
Hemoglobinopathy
Retic increased
B.M. Exam
Ring Sideroblasts
Sideroblasts
Anemia
Acquired / Congenital
Decreased Increased
IDA
Blood loss
Anemia of chronic
Infection
TIBC N / decreased
Retic increased
History
Stool Exam
Etiology of Iron Def.
 Requirements – periods of rapid growth
  Availability –poor diet, poor source
  Absorption : GI diseases
 Losses : Pregnancy, Lactation, Menstruation,
Ext. Bleeds
GI : Polyp, Piles, Fissure, Worms, Meckel,
Varices
Vicious Cycle
• Top fed infant – bottle
• Improper BF
• Poor weaning
• Cow’s milk
• Recurrent infections
• Worms, Malaria
Iron Stores
• Hemoglobin –70%
• Myoglobin
Enzymes
• Storage Iron
– 4-5% earth’s crust is iron
– Child – 70 mg/kg
– Male – 4.0 gms, Female – 3.0 gms
Clinical Manifestations
• Multisystemic disease
• Hematological – Anemia
• Muscles, Cerebral Cortex, Epithelial tissues,
Myocardium, Peri. nerves, Kidney, Liver,
Immune system
Non - Hemat. Manifestations
• Neurological: Intellect, Cognition, Behavioural
changes
• Epithelial (rare in children)
• Tongue: Glossitis, Chelosis
• Nail: Platynychia / Koilonychia
• Esophageal: Webs
• Exercise intolerance
• Immune dysfunction
Anemia History - Diet
• Prolonged bottle feeding - improper weaning
• Cow's milk - IDA, Goat's milk - Folate deficiency
• H/o Pica - cause & effect both
• Food fads in adolescents
• Exclusively breast-fed babies do not develop IDA till
6 months of age
Laboratory Diagnosis IDA
• Screening tests :
RBC compartment
– Hb, PS, RBC Indices, RDW
• Confirmatory tests :
Plasma/storage compartment
– S.Iron, TIBC, Transferrin saturation
– S.Ferritin, B M iron staining
When to suspect IDA ?
• During period of growth / food fads
• Bottle-fed, Cranky child, Pica
• Associated chronic bleeding / Worms
• Microcytic, hypochromic anemia
• Low iron status / S.Ferritin
• High RDW
• HbA2 - N (Repeat after iron therapy)
When to suspect β-Thal. Minor ?
• High index of suspicion / community
• Hypochromic / Microcytic with normal iron status
/ RDW
• Inadequate response to iron treatment
• Reticulocytosis, Polychromasia
• Basophilic stippling
• HbA2 in Hb electrophoresis
Treatment
• Making Correct diagnosis
• Diet modification
• Treat the cause
• Iron supplementation
• Prevention
Oral Iron Therapy
• Dose: 3-6 mg/kg of elemental iron
• Divided in 1-2 doses
• On empty stomach –ideal
On full stomach if intolerance
• Duration : 3 mo after Hb has normalised
• Daily Vs twice a week therapy
Oral Iron Side Effects
• Nausea, Vomiting, Pain in abdomen, Diarrhea,
constipation
• Discoloration of stool
• Staining of tongue / teeth
• Rarely poisoning in higher doses
• True intolerance rare
Failure of Oral Iron
• Wrong diagnosis
• Wrong formulation
• Wrong dosage
• Poor compliance
• Poor diet
• Basic cause not treated
esp. bleeding
Monitoring of Response
• Subjective well being
• Retic 8-10 % at day 7
• Replenishment of iron enzymes
• Hb es by 1 gm/dl/week
Normal by 2-3 mo.
• PS mixed population
• Indices : 2-3 mo to normalise
• Epithelial changes : 2-3 mo.
Macrocytic Anemia - Blood & Marrow Morphology
Megaloblastic
(Clinical Data, Serum Vitamins)
Folate Deficiency
No Deficiency
Congenital Disease
Drugs
B12 DEF
Diet
Schilling’s Test
With Intr. Factor
Corrected
Pern. Anemia
Gastric Resection
Ingestion Of Corrosives
Inert. Intr. Factor
Non-corrected
Small Bowel Bact
Fish Tapeworm
Familial B12 Malab
Drug Induced Malab
Ileal Disease
Diet
Good
Drug Ind. Malab
Jejunal Resect
Trop. Sprue
Gluten Sensitivity
Poor
Dietary Def
Pregnancy
Infancy
Certain Blood
Diseases
Macrocytic Anemia - Blood & Marrow
Morphology
Non - Megaloblastic
Reticulocytes
Increased
Hemolytic Anemia
Hemorrhage
N or Decreased
Alcoholism
Hepatic Dis
Meylody’s Anemia
Hypothyroid
COPD
Megaloblastic anemia etiology
• Folate deficiency: Mainly nutritional, Food fads,
Goat’s Mlik (poor in folate), Malabsorption, drugs
(antimetabolites)
• B12 deficiency: Mainly dietary food fads, pure
vegan, worms, rarely Pernicious anemia in
children
• Rare: Congenital – enzyme deficiency
• Orotic aciduria
Investigations
• CBC: Macrocytic anemia with high RDW
• PS: Macrocytic, ovalocytosis, basophilic stippling,
polychromasia, Howell Jolly bodies
• Increased indirect bilirubin, high LDH
• Bone marrow: Megaloblastic changes
Treatment
• Oral folic acid: 1-5 mg/day for 3-6 mo
• Oral B12: 10 mcg/Kg/day for 3-6 mo
• Give both folate and B12, B12 deficiency treated
only with folate – Hb will raise but CNS changes
will worsen
• If pernicious anemia: Injectable B12 – initially 1 mg
daily IM for 2 weeks followed by 1 mg monthly life
long
• Deworm, improve diet
Response to treatment
• Bone marrow may totally revert in 24 hours
• Patient starts feeling well in days
• Retic response will peak at 5-7 days
• Hb starts rising after 1-2 weeks
• Hb normalizes by 3 months
• PS becomes normal after 1-2 months as old
macrocytic RBCs will persist till their life
Treat the Cause
• Breast feeding advice
• Proper weaning
• Avoid bottle feeding
• Restrict top milk intake
 calories in diet
• Improve type of diet
• De-worming
• Treat GI dis, bleeding
Prevention of Anemia
• Diet modification
• Iron supplementation
• Food fortification
• Control infections, worms
• National programs and schemes
Common Iron rich foods
• Green leafy vegetables:Chick pea, spinach,
amaranth, mint, mustard leaves
• Lentil, grams, fresh fruits
• Mutton
National Programmes
• ICDS
• Mid day Meal Scheme
• Nutritional programme for adolescent girls
• Weekly Iron Folic acid Supplementation
• National Iron + Initiative
Thank you

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Nutritional Anemia.ppt

  • 2. Definition • Reduction in oxygen carrying capacity of blood as a result of decreased : – Red cell mass – Red Cell count / HCT – Hb concentration
  • 3. WHO cutoffs for Anemia Age group Hemoglobin (Hb) Hematocrit (PCV) 6 Mo to 5 yr <11.0 <33 5 – 11 Yr <11.5 <34 11 – 13 Yr <12.0 <36 Non pregnant women <12.0 <36 Men <13.0 <39
  • 4. Problem Burden • Anemia is a global public health problem especially in south east asia, africa and south america • Nutritional anemia -major public health problem in India • 7 out of every 10 children aged 6-59 months are anemic in India
  • 5. Classification • Aetiological – ↓Production: e.g. aplastic anemia – Hemolysis: e.g. G6PD deficiency – Hemorrhage: e.g. rectal polyp • Rate of onset – Acute: e.g. malaria with hemolysis – Chronic: e.g. Iron deficiency anemia • Severity – Mild 10 gm % – Moderate 7-10 gm% – Severe < 7 gm%
  • 6. Nutritional Anemia • Iron • Folic acid • Vit. B12 • Others: Protein, Zinc, Copper, Vit. C • Deficiency of any of these will lead to a chronic state of nutritional anemia
  • 7. Approach To Any Anemia • Detailed History • Detailed head to toe examination • Screening laboratory tests • Confirmatory tests
  • 8. Anemia - History • Age / Sex / Inheritance • Infections & Worms • Drugs • Diet, Pica • Community
  • 9. History in Nutritional anemia • Symptoms of anemia: Fatigue, shortness of breath, lassitude, weakness, Dyspnea on Exertion • Age of onset: 6 mo-36 months • Sex: Both sexes equally affected in childhood, after adolescence females > males • Diet: Lack of breast feeds, excess of milk based diet, bottle fed, poor weaning food, predominantly vegetarian diet, pure vegan (B12 def.)
  • 10. History in Nutritional anemia – Contd.. • H/O Pica: Altered appetite for mud, chalk, pencil, color, raw food items etc. – Both cause and effect • H/O irritability, crankiness, stubbornness, listlessness • H/O breath holding spasms, • Infections: Common as a cause of anemia, rule out worms infestation esp. hook worm, round worms, giardia,
  • 11. Anemia – Physical Exam • Signs of anemia: Pallor, Puffiness, Edema feet, hemic murmer • Tongue: Pallor, Bald & shining tongue, loss of papillae, Angular cheilosis (IDA) • Nails: Platynychia, Koilonychia (IDA) Hyperpigmented knuckles (Megaloblastic anemia) • Fidgety, irritable, cranky, listless child, • Resents strangers and examination
  • 12. Common Manifestations Loss of Papillae Pale & Bald tongue Platynychia Hyperpigmented knuckles
  • 13. Anemia – Physical Exam – Contd.. • To rule out other causes of anemia look for: • Abnormal facies (e.g. Hemolytic facies) • Hepatosplenomegaly (e.g. Thalassemia) • Lymphadenopathy (infections, TB, malignancies) • Bony tenderness (e.g. leukemia) • Petechiae/purpura (aplastic anemia, leukemia) • Weight loss (malignancies) • Skeletal changes (e.g. Fanconi’s anemia)
  • 14. Laboratory Investigations • Screening tests – Hb, HCT – Red cell indices – Reticulocyte count – P.S. examination • Confirmatory tests
  • 15. RDW values in various diseases RDW Low MCV Normal MCV High MCV Normal Thalassemia trait Normal Aplastic anemia High IDA Chronic liver disease, malignancies, myelofibrosis, myelotoxic drugs Megalo. An., Imm. Hem. An.
  • 16. Reticulocyte Count • Count 500 cells - supravital staining • Normal : 1-2% • Low count: BM depression like aplastic anemia, BM infiltration, PRCA • High count: Good BM response like in hemolysis, hemorrhage, post-treatment
  • 17. Advantages of PS examination • Bedside, easily available • Cost effective, Imp. Info. • Types of anemia • At times diagnostic • ↓need for further tests
  • 18. PS examination Normocytic Normochromic Macrocytic – Megaloblastic anemia Microcytic Hypochromic – IDA Microcytic Hypochromic – Thalassemia (Target cells, NRs)
  • 19. Blood Film Red cell Indices Hypochromic Microcytic MCV < 80μ3 MCH < 29 ρg MCHC < 32 % Normocytic Microcytic MCV 75-95 μ3 Morphological Classification Macrocytic MCV > 95μ3
  • 20. Microcytic, Hypochromic Anemia D.D. MCV < 80μ3, MCH < 29 ρg., MCHC < 32% • IDA • Hemoglobinopathies • Anemia of chronic infections • Sideroblastic Anemia • Lead poisoning
  • 21. PS Exam. / Red Cell indices Hypochromic Microcytic Anemia MCV < 80u3, MCH < 20 Pg., MCHC < 32% Normal / Decreased Normal / Increased Sr. Iron Iron Store, Sr. Ferritin Abnormal Normal Hemoglobinopathy Retic increased B.M. Exam Ring Sideroblasts Sideroblasts Anemia Acquired / Congenital Decreased Increased IDA Blood loss Anemia of chronic Infection TIBC N / decreased Retic increased History Stool Exam
  • 22. Etiology of Iron Def.  Requirements – periods of rapid growth   Availability –poor diet, poor source   Absorption : GI diseases  Losses : Pregnancy, Lactation, Menstruation, Ext. Bleeds GI : Polyp, Piles, Fissure, Worms, Meckel, Varices
  • 23. Vicious Cycle • Top fed infant – bottle • Improper BF • Poor weaning • Cow’s milk • Recurrent infections • Worms, Malaria
  • 24. Iron Stores • Hemoglobin –70% • Myoglobin Enzymes • Storage Iron – 4-5% earth’s crust is iron – Child – 70 mg/kg – Male – 4.0 gms, Female – 3.0 gms
  • 25. Clinical Manifestations • Multisystemic disease • Hematological – Anemia • Muscles, Cerebral Cortex, Epithelial tissues, Myocardium, Peri. nerves, Kidney, Liver, Immune system
  • 26. Non - Hemat. Manifestations • Neurological: Intellect, Cognition, Behavioural changes • Epithelial (rare in children) • Tongue: Glossitis, Chelosis • Nail: Platynychia / Koilonychia • Esophageal: Webs • Exercise intolerance • Immune dysfunction
  • 27. Anemia History - Diet • Prolonged bottle feeding - improper weaning • Cow's milk - IDA, Goat's milk - Folate deficiency • H/o Pica - cause & effect both • Food fads in adolescents • Exclusively breast-fed babies do not develop IDA till 6 months of age
  • 28. Laboratory Diagnosis IDA • Screening tests : RBC compartment – Hb, PS, RBC Indices, RDW • Confirmatory tests : Plasma/storage compartment – S.Iron, TIBC, Transferrin saturation – S.Ferritin, B M iron staining
  • 29. When to suspect IDA ? • During period of growth / food fads • Bottle-fed, Cranky child, Pica • Associated chronic bleeding / Worms • Microcytic, hypochromic anemia • Low iron status / S.Ferritin • High RDW • HbA2 - N (Repeat after iron therapy)
  • 30. When to suspect β-Thal. Minor ? • High index of suspicion / community • Hypochromic / Microcytic with normal iron status / RDW • Inadequate response to iron treatment • Reticulocytosis, Polychromasia • Basophilic stippling • HbA2 in Hb electrophoresis
  • 31. Treatment • Making Correct diagnosis • Diet modification • Treat the cause • Iron supplementation • Prevention
  • 32. Oral Iron Therapy • Dose: 3-6 mg/kg of elemental iron • Divided in 1-2 doses • On empty stomach –ideal On full stomach if intolerance • Duration : 3 mo after Hb has normalised • Daily Vs twice a week therapy
  • 33. Oral Iron Side Effects • Nausea, Vomiting, Pain in abdomen, Diarrhea, constipation • Discoloration of stool • Staining of tongue / teeth • Rarely poisoning in higher doses • True intolerance rare
  • 34. Failure of Oral Iron • Wrong diagnosis • Wrong formulation • Wrong dosage • Poor compliance • Poor diet • Basic cause not treated esp. bleeding
  • 35. Monitoring of Response • Subjective well being • Retic 8-10 % at day 7 • Replenishment of iron enzymes • Hb es by 1 gm/dl/week Normal by 2-3 mo. • PS mixed population • Indices : 2-3 mo to normalise • Epithelial changes : 2-3 mo.
  • 36. Macrocytic Anemia - Blood & Marrow Morphology Megaloblastic (Clinical Data, Serum Vitamins) Folate Deficiency No Deficiency Congenital Disease Drugs B12 DEF Diet Schilling’s Test With Intr. Factor Corrected Pern. Anemia Gastric Resection Ingestion Of Corrosives Inert. Intr. Factor Non-corrected Small Bowel Bact Fish Tapeworm Familial B12 Malab Drug Induced Malab Ileal Disease Diet Good Drug Ind. Malab Jejunal Resect Trop. Sprue Gluten Sensitivity Poor Dietary Def Pregnancy Infancy Certain Blood Diseases
  • 37. Macrocytic Anemia - Blood & Marrow Morphology Non - Megaloblastic Reticulocytes Increased Hemolytic Anemia Hemorrhage N or Decreased Alcoholism Hepatic Dis Meylody’s Anemia Hypothyroid COPD
  • 38. Megaloblastic anemia etiology • Folate deficiency: Mainly nutritional, Food fads, Goat’s Mlik (poor in folate), Malabsorption, drugs (antimetabolites) • B12 deficiency: Mainly dietary food fads, pure vegan, worms, rarely Pernicious anemia in children • Rare: Congenital – enzyme deficiency • Orotic aciduria
  • 39. Investigations • CBC: Macrocytic anemia with high RDW • PS: Macrocytic, ovalocytosis, basophilic stippling, polychromasia, Howell Jolly bodies • Increased indirect bilirubin, high LDH • Bone marrow: Megaloblastic changes
  • 40.
  • 41. Treatment • Oral folic acid: 1-5 mg/day for 3-6 mo • Oral B12: 10 mcg/Kg/day for 3-6 mo • Give both folate and B12, B12 deficiency treated only with folate – Hb will raise but CNS changes will worsen • If pernicious anemia: Injectable B12 – initially 1 mg daily IM for 2 weeks followed by 1 mg monthly life long • Deworm, improve diet
  • 42. Response to treatment • Bone marrow may totally revert in 24 hours • Patient starts feeling well in days • Retic response will peak at 5-7 days • Hb starts rising after 1-2 weeks • Hb normalizes by 3 months • PS becomes normal after 1-2 months as old macrocytic RBCs will persist till their life
  • 43. Treat the Cause • Breast feeding advice • Proper weaning • Avoid bottle feeding • Restrict top milk intake  calories in diet • Improve type of diet • De-worming • Treat GI dis, bleeding
  • 44. Prevention of Anemia • Diet modification • Iron supplementation • Food fortification • Control infections, worms • National programs and schemes
  • 45. Common Iron rich foods • Green leafy vegetables:Chick pea, spinach, amaranth, mint, mustard leaves • Lentil, grams, fresh fruits • Mutton
  • 46. National Programmes • ICDS • Mid day Meal Scheme • Nutritional programme for adolescent girls • Weekly Iron Folic acid Supplementation • National Iron + Initiative

Editor's Notes

  1. Nutritional anemia is caused when one or more factors required for the formation of hemoglobin are not available. Bone marrow can be compared to a factory manufacturing some goods. Nutritional anemia is like lack of raw materials required for factory.
  2. History in a case of nutritional anemia:
  3. Points in history in a case of nutritional anemia
  4. Physical examination in a case of nutritional anemia will show the signs of anemia, signs specific to nutritional cause esp. in tongue and nails.
  5. It is equally important to look for presence of signs that may suggest non-nutritional cause of anemia like organomegaly, skeletal changes, abnormal facies, weight loss etc.
  6. Iron deficiency is caused by decreased iron intake in food esp. with excess milk intake and bottle feeding with poor weaning. Other causes are decreased absorption like short bowel, increased demands like during growth period and increased losses like in GI hemorrhages.
  7. Most common cause of iron deficiency is an infant with poor food intake, excess top milk intake, bottle feeding, lack of breast feeding, poor weaning and repeated infections, worms etc.
  8. Iron is required not only for hemoglobin but also in other iron dependent proteins and enzymes like myoglobin and enzymes in brain. It is sad that though mankind is surrounded with abundant iron in atmosphere, iron deficiency is the most common deficiency seen in humans.
  9. Accordingly iron deficiency not only leads anemia but it also leads to fatigue (Myoglobin affection), CNS changes (Brain enzymes affected), and repeated infections (immune system affection).
  10. While anemia will get corrected with iron therapy, cognitive dysfunction can be permanent in spite of iron therapy. This can explain CNS chanes like irritation, epithelial changes etc. as iron is widely required by many system in body.
  11. While there is no need to do iron studies in every case of iron deficiency, s. iron will low, s. TIBC will be high and TS will be low. TS < 12 is diagnostic if iron deficiency. While iron studies can be affected by oral intake, S. ferritin directly reflects the iron stores. S. ferritin less than 20 ng/ml is suggestive of iron deficiency.
  12. Treatment if iron deficiency include correct diagnosis, oral iron therapy, diet improvement, treatment of the cause and prevention.
  13. Oral iron therapy protocol.
  14. Common side effects following iron therapy. However pre-starting counseling of parents will help the parents cope with the side effects. The GI upset can be minimized by starting with low dose and gradually increasing the dose, and by taking the dose with meals.
  15. Common causes of iron failure.
  16. Points to remember while following up iron therapy.
  17. Common causes for megaloblastic anemia
  18. Investigations will show macrocytic anemia with high MCV, typical PS with macro-ellipto cytic anemia. There is ineffective erythropoiesis in megaloblstic anemia and hence there is increased indirect s. bilirubin and high LDH. Bone marrow is diagnostic with megaloblastic erythropoiesis.
  19. Pictures of macrocytis anemia on PS, Hypersegmented neutrophil on PS, Basophilic stippling on PS, presence of Howell Jolly body on PS and BM showing Megaloblasts.
  20. Treatment of megaloblastic anemia includes oral supplements with both folate and B12 as in children most common cause is dietary. If only folates are given and if the cause is B12 deficiency, the anemia will be corrected but the CNS changes will deteriorate.
  21. It is important to do bone marrow BEFORE instituting specific therapy or blood transfusions and the changes may revert totally normal within 24 hrs of such therapy.
  22. In nutritional anemia unless you traet the cause of anemia, the anemia will recurr when the therapy is stopped e.g. dietary improvement, stopping bottle feeding etc.
  23. Prevention is caused by diet modifications, food fortifications and prophylactic supplements. Food fortification has been tried with iron fortified salt. However it changes the color of the food.
  24. National anemia control program was initially anemia prevention program , however it has not made much dent in the iprevalence of iron deficiency. Hence iot has been converted to control program Under this children < 5 yrs and would be mothers are targeted on a priority with at least 100 days of oral iron supplements per year in the form of IFA (Iron Folic Acid Tablets). In pediatric patient IFA containing 20 mg elemental iron and 100 mcg of folate and adult tablet contains 100 mg elemental iron and 500 mcg folate.