Short description for Iron deficiency anemia in children, etiology and how to manage it. Oral & parenteral form of treatment also included here

2. ANEMIA:
What is anemia?
Ans Reduction of Hb conc in relation to age, sex.
Definition: Anaemia refers to reduction of Hb conc.,
hematocrit or number of red blood cell (RBC) mass less than
normal, determined by > 2 standard deviations below the
normal mean for age & sex
Anemia is not a disease, but an expression of an underlying
disorder or disease.

3. The word
"anemia" derives
from an ancient
Greek
word anaimia, me
aning "lack of
blood."

4. Normal level: depends on age –
Normal range varies with age, so anemia can be defined according to
age as :
  Neonate: Hb <14g/dl
  1-6 months: Hb <11.5 g/dl
  6 months-2 years: Hb <12
g/dl.
  2 to 6 years: Hb <12.5 g/dl
  >6 to 12years: Hb <13.5 g/dl
What are the normal level of Hb in children?
Hb conc (g/dl)
12- 18 yrs: Male: <14.5 Female:14
>18 yrs: Male: 15.5 Female:14 Philip 6th, p
711

5. Types: (According to severity)
Anemia may be mild, moderate, or severe in nature.
Classification Hb (g/dl) Features
Mild anemia 9.5-11 often asymptomatic and
frequently escapes detection.
Moderate anemia 8-9.5 may present with other symptoms and
warrants timely management to
prevent long-term complications.
Severe anemia < 8 will warrant investigation and prompt
management.

6. IRON DEFICIENCY ANEMIA
Definition: IDA is a condition in which there is confirmed evidence of
deficiency of iron in blood and bone marrow analysis.

7. IRON DEFICIENCY ANEMIA
 Most commonest cause of anemia in children
 Most common age group: 6-24 months
 Prevalence of iron deficiency (ID) is twice as high as IDA.
 Incidence:
 Infancy: high incidence
 Under 5 years: 40-50%
 School going children age 5 to 8 years: 5.5%
 Pre-adolecence: 2.6%
 Pregnant teenage girl : 25%
 No socio-economic group is spared.

8. IRON DEFICIENCY ANEMIA
 Most common cause of anemia in children
 Most common age group: 6-24 months
 Sources of iron:
Animal source: (heme iron)
meat, liver, fish and poultry.
Plant source: (non-heme iron)
beans, pulses, tubers, dried fruits & green vegetables (spinach,
brocoli)
Which one better?
animal source, as it is readily absorbed (15-30%) and absorption is
not influenced by other dietary factors.
On the other hand plant source absorbed only 2-20%.

10.  Daily requirement: 10 mg elemental iron
 Daily 1 mg iron must be absorbed for maintaining children’s positive
iron balance
 Site of absorption: duodenum & jejunum
 Absorption form: ferrous form
 Stored form: ferritin, haemosiderin
 Factors influence iron absorption:
• Enhanced by: vitamin C, proteins
• Decreased by: Phylates (unrefined cereals), tannins (tea,
legumes), phosphates (found in egg), polyphenols (coffee, spinach
etc), calcium, fibres
Physiology of Iron:

11. Aetiology of IDA
 Decreased iron stores:
pre-term, LBW, small for age, twins,
 Decreased intake: most common cause
Delayed weaning, iron poor diet
 Decreased absorption:
PEM, malabsorption syndromes, chronic diarrhea or persistent/recurrent diarrhea
post surgery (gastrectomy or gastro-enterostomy)
 Increased losses: most important cause
GI bleeding, hookworm infection, PUD, bleeding diathesis,
Meckels diverticulitis, polyp, anal fissure, haemorroid, hemangioma or IBS
 Increased demand:
prematurity, LBW, recovery from PEM, adolescence
(for adult- pregnancy, lactation, menstruation)

13. Maternal cause
 Babies born to mothers with unusual perinatal hemorrhages
 Lactation failure
 Inappropriate weaning (with cow’s milk, sagu, suzi, rice gruel etc as they
are deficient iron)
Others:
 Early clamping of umbilical cord (within <30 sec; neonatal case)

14. Stages of IDA
 Stage 1: Negative iron balance (depleted iron stores)
a. Inadequate intake
b. Rapid growth of infant & children
c. Pregnancy
d. Blood loss
 Stage 2: iron deficient erythropoiesis
complete deficient of iron stores, S Ferritin <15 µg/L µ
 Stage 3: iron deficiency anemia
- gradual fall of Hb & Hct results, hypochromic, microcytic anemia with other RBC
dysmorphology
- As a consequence of prolong iron depletion, erythoid marrow become hyperplasia > tissue
became changed due to decreased intracellular level of iron dependent enzymes.
reduced level of S ferritin & decreased
stainable iron on bone marrow

16. Assessment:
Diagnosis is made by:
Patient’s history
Patient’s physical examination
Haematological lab findings
Inv. to exclude other disease.
Identification of cause of IDA or any anemia is important so that appropriate
therapy is used to treat the anemia.

17. Patient’s History:
 Dietary history – dietary habits, esp iron, folate, malnutrition
Very important for IDA
 Drug history – present or past
 h/o Blood loss – acute or chronic
eg GI bleeding, hematuria, black stools
 Family h/o hemolytic disease, bleeding disorder
 Description & duration of symptoms
[Moderate to severe anemia – weakness, lethargy, fatigue, palpitations,
shortness of breath, symptoms of cardiac failure ]
 Possible exposure to chemical and/or toxins

18. Physical examination:
Signs:
 Pallor – conjunctival mucosa, nail bed, palms, soles
 Features of Hyperdynamic circulation: tachycardia, bounding pulse,
cardiomegaly, systolic murmur (particularly apical)
 Features of congestive heart failure may be present in more severe anemia
 Specific signs:
 Koilonychia: iron deficiency anemia
 Jaundice: hemolytic anemia
 Hepatosplenomegaly: thalassemia, leukemia
 Bone deformity: thalassemia, other congenital anemia
 Bleeding or coagulation disorder: anemia with excess bruising

19. Koilonychia: spoon shaped nails

20. Special features for IDA:
 PICA: increased desired to have unusual substances e.g. mud, brick, dirt, rubber etc.
 Features related to impaired neuro-cognitive function -
 Irritability
 Poor mental and motor developmental growth (Bayley scale)
 Shorter attention span, Decreased school performances
 Breath holding spells (when young children stop breathing for up to 1 minute and often cause the child to
lose consciousness)
 Increased risk of seizures.
 Features related to atrophic changes in epithelium of
a. Mouth, lips: cracking
b. Tongue: atropic glossitis ( atrophy of papillae, smooth, pale & shiny tongue)
c. Angle of mouth: redness, soreness and cracking
d. Pharynx, esophagus: dysphagia [ Plummer-Vinson syndrome]
e. Nails: koilonychia, flattening & thinning of nails.
 Reduce immunity & frequent infections – a

21. INVESTIGATIONS:
 Complete blood count (CBC)
 RBC count with Hb, Hct, & Reticulocyte count
 RBC indices: MCV, MCH, MCHC, RDW (red cell distribution width)
 WBC count total and differential
 Platelet count
 Cell morphology – peripheral blood film
 Iron profile –
 Serum iron
 Ferritin
 TIBC
 Bone marrow study - iron stain

22. Investigation findings >>
Complete blood count (CBC)
RBC –
• Hb, Hct: below the acceptable level for age.
• Reticulocyte count usually normal or elevated.
RBC indices:
• MCV, MCH, MCHC, - lower than normal
• RDW (red cell distribution width) = widened [>14.5%] (normal or low in
Thalassemia)
WBC count total and differential: normal
Platelet count: normal or increased (occasionally)
Cell morphology: (blood smear):
microcytic hypochromic with anisocytosis and poikilocytosis, tear drop cell, pencil
shaped cell. In severe cases target, elliptical, oval shaped cell.

25. Iron profile –most confirmatory test
Serum iron: ↓↓ decreased (<10 µmol/L) [not diagnostic]
Ferritin: ↓↓ decreased (<12 ng/ml or 12 µg/L; is considered diagnostic for
IDA)
Total Iron Binding Capacity (TIBC): high (80 µmol/L or more)
Serum soluble transferrin receptor level (STfR): ↓↓ decreased
Transferrin saturation: ↓↓ decreased
Free erythrocyte protoporphyrin (FEP): raised
Percentage saturation of Iron binding protein: decreased, below 16%
If doubtful about ferritin level due to presence of infection as it acting as
acute phase protein STfR will make it clear because its not influenced by IL6
as it influences ferritin

26. Bone marrow:
 Method– biopsy (preferred) or aspiration
 Findings-
Erythroid hyperplasia
Macronormoblastic erythropoiesis, the predominant cells are polychromatic
normoblasts which are usually smaller than normal. Poorly hemoglobinized
pyknotic normoblasts are seen.
Leukopoiesis and thrombopoiesis are normal
 Decreased or absent stainable iron (by Prussian blue stain)
Sideroblasts are decreased (by potassium ferrocyanide staining)

27. This images show iron
stains for comparison.
In image (1) iron is
increased, as
demonstrated by large
amount of blue material.
Images (2) & (3) show
decreasing amounts of
iron.
Image (4) shows no iron.
Prussian blue (iron) stained bone marrow
1
1
- This test is considered the gold standard for evaluating marrow iron stores.
4
3
2

28. Other Tests:
 Stool RE for ova of hookworm
 Stool for OBT
 Urine RE for RBC
 Other tests according to presentation

29. Differential Diagnosis
 Thalassemia
 Anemia of chronic disease
 Lead poisoning
 Sideroblastic anemia

30. Comparison between different types of anemia
IDA Thalassemia Anemia of chronic
disease
Sideroblastic anemia
A. Smear - microcytic hypochromic
B. Red cell indices
MCV, MCH,
MCHC
Reduced Reduced Low normal Cong type: very low
Acquired type: MCV often raised
C. Biochemistry (serum)
Iron Reduced Normal Reduced Normal or increased
Ferritin Reduced Normal Normal or increased Normal or increased
TIBC Increased Normal Normal or increased Normal
Percentage
saturation
Reduced Normal Reduced Normal or increased
D. Hemoglobin studies for thalassemia
E. Bone
marrow
studies
Ring sideroblast
[iron appears as a ring round
the nucleus of normoblast]
(Prussian blue positive)

31. Management:
 Acute anemia usually warrants immediate medical attention
 Treatment depends on the severity and underlying cause of anemia
Objectives of IDA treatment
 Restore Hb level to normal
 Replenish the depleted iron stores and
 Treat underlying causes
Rx includes -
 Specific treatment
 Counsel parents about cause, consequences and importance of treatment and prevention
of IDA
 Supportive measures, such as supplemental oxygen for decreased oxygen carrying
capacity, fluid resuscitation for hypovolemia and bed rest or activity restriction for fatigue,
may be required.

32. Specific treatment:
 Nutritional counseling – Breast milk feeding with complementary diet
a. diets are rich in iron, iron fortified infant formula or cereals [ no cow’s milk until 1st year of age]
b. avoidance of food deficient of iron,
c. avoidance of foods those interfere with iron absorption.
d. facilitators of iron absorption e.g. Vit C rich foods should included
 Iron therapy:
a. Oral form:
b. Parenteral form: IV or IM
 Periodic deworming
 Blood transfusion –
--PRBC (with signs of cardiac dysfunction& Hb level ≤4 g/dl
-- Exchange transfusion ( with congestive heart failure)

33. Iron conc. in different milk -
Type Iron conc. Absorption
rate
Breast milk 1.5 mg/L 50%
Infant
formula
5-9 mg/L 10%
Cow’s milk 0.5 mg/L 10%
Iron conc. In different food
High iron
content
Average iron content
• Red meat,
(beef, lamb,
liver, Kidney)
• Fish
• Egg yolk
• Pulses, bean, peas
• Dark green vegetables (e.g.
broccoli, spinach, banana, red
shakh, mashroom)
• Dried fruits e.g. Dates
• Nuts & seeds
AH Molla 207

34.  Ferrous sulphate:
adult dose: 400-600 mg/day in divided doses
prophylactic: 200 mg/day
 Ferrous Gluconate:
 Ferrous fumerate:
 Ferrous ascorbate
 Ferrous lactate
 Ferrous succinate
 Ferrous glycin sulphate
 Iron polymaltose complex (Compiron)
adult: 1 cap/day child (syp or drop):
Side effect:
• Black stool (guiac negative stool or
unabsorbed iron)
• Diarrhoea/ constipation
Treatment failure --
• Poor compliance –
• Blood loss
• Absorption problem
• Celiac disease

35. Indication:
 Poor or Intolerance of iron or failure of oral iron therapy
 Poor patient’s compliance
 Chronic diarrhoea
 Bleeding from GIT ( which aggravated by oral iron), severe
bowel disease (celiac disease, atrophic gastritis), gut
surgery.
 Severe iron deficiecny requiring rapid replacement of iron
stores as substitute of Blood trasnsfusion
 Iron deficiency in heart failure
 Genetically induced IRIDA
Side effects/ complication:
Hypersensitivity reaction (rarely)
Flushing, headache, muscle & joint pain, nausea, dizziness,
fever & chills
Intra muscular:
• Iron Dextran
(approved by FDA for children)
Intravenous:
• Na ferric gluconate
• Iron sucrose

37. Mansour, D., Hofmann, A. & Gemzell-Danielsson, K. A Review of ClinicalGuidelineson the Management of Iron Deficiencyand Iron-Deficiency Anemia in Women with Heavy Menstrual Bleeding. Adv Ther 38, 201–225 (2021). https://doi.org/10.1007/s12325-020-01564-y

38. Response to iron therapy in IDA:
MR khan301
After initiation
of treatment -
Response
12-24 hours Replacement of intracellular iron enzymes, subjective
improvement, decreased irritability, and increased appepite.
36-48 hours Initial bonemarrow response, erythroid hyperplasia
48-72 hours Reticulocytosis, peaking at 5-7 days
4-30 days Increase in hemoglobin level
1-3 months Repletion of stores
• Hb level should rise 1 gm/dl by every10 days after a lag period of 7-10 days.
• If this rise does not happen, the possibilities of blood loss, infection, renal failure, folic acid
deficiency or thalassemia should be considered

39. How you know the Pt is responding on treatment?
Ans -By observing reticulocyte count with expected reticulocyte response.
If reticulocyte response less than 2 or 3 times normal indicates an inadequate
marrow response .
Reticulocyte (%) can be corrected to measure the magnitude of the marrow
production in response to anemia are as follows -
Reticulocyte production index= reticulocyte (%) X (observed hematocrit/ normal hematocrit)X
1/µ
Here
 Normal Reticulocyte production index -- 1.0
 In chronic hemolytic anemia -- >2.5
 Maximum marrow response – 6-8

40. How Hookworm infection can cause iron
deficiency anemia?
 IDA can be happened because when hookworm attach in intestinal mucosa, releases
coagulases, causing ongoing blood loss in stool, and also consumption of blood by parasite.
 Hookworm infection, caused by parasites belonging to the species Necator americanus and
Ancylostoma duodenale, is most commonly transmitted through contact with contaminated soil,
although oral ingestion of larvae is also possible.
 Diagnosis is traditionally established by stool examination, though this method is insensitive, and
serial examinations may be needed to make the diagnosis.
 How you suspect?
-- Evidence from stool examination + unexplained eosinophilia
- Usually, eosinophilia is mild and varies over course of disease, increased after 2-3 weeks and peaked at 5-9 weeks.
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41. Prognosis
Prognosis of anemia varies based on the cause of anemia.
Other factors contributing to the prognosis include:
1. Age of the patient:
- Elderly patients have a poor prognosis due to their advanced age, malnutrition, and multiple comorbidities.
1. Severity of anemia - Hb <6.5 g/dL is life-threatening and can cause death.
2. Duration of anemia
3. Comorbidities
4. Access to medical care
5. Diet
Complications
 Untreated anemia can be life-threatening and can even cause death.
 Anemia results in a decreased oxygen-carrying capacity of blood. In short term, body can compensate with
an increase in heart rate and respiratory rate. If left untreated, anemia can cause multi-organ failure. This
can include high output heart failure, angina, arrhythmias, cognitive impairment, and renal failure, among
others. In pregnant women, untreated anemia can cause premature birth and low birth weight.