Anemia in Children


By: Dr.Abera Olani
.
(MD, pediatrician)

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 Content

Definition.
Classification /Approach.
IDA.
Physiologic Anemia of infancy.
Megaloblastic Anemia.

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 
 Anemia is defined as a reduction of the red blood cell (RBC) volume
or hemoglobin concentration below the range of values occurring in
healthy persons.

 It is not a specific entity as it is caused by different underlying

pathologies.

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 
In practice, anemia most commonly defined by reduction in one or both of
the following:-
Hematocrit( Hct):- this is the fraction volume of a whole blood
sample occupied by RBC & is expressed by percentage.

Hemoglobin (Hgb):- this is a measure of the concentration of the

RBC pigment hemoglobin in whole blood ,expressed as gram per
100ml(dl).

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 
 The age variation for Hgb and RBC size changes with age pronounced in
the pediatrics population thus is important to use age & sex adjusted norms.

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 Physiologic adjustments of anemia


 Increased cardiac output.
 Increased oxygen extraction (increased arteriovenous oxygen difference)
 Shunting of blood flow toward vital organs and tissues.
 Concentration of (2,3-DPG) increases within the RBC.
 Increased EPO production.

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 Important diagnostic considerations

 Important to see other cell lines ( Aplastic anemia, malignancy).
 MCV very useful.
 Check for reticulocyte count.
 Reticulocytopenia impairment of normal erythropoiesis,
 Reticulocytosis ongoing bleeding or hemolysis.
 Increased indirect hyperbilirubinemia and LDH with Reticulocytosis tells
hemolysis.
 RBC peripheral morphology very important.
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 CLASSIFICATIONS OF ANEMIA


 Etiological classification.
 Classification based on severity.
 mild anemia (Hgb 9.0–10.9 g/dL)
 moderate anemia (Hgb 7.0–8.9 g/dL),
 severe anemia (Hgb less than 7.0 g/dL).
 Acute- develops over days.
 Chronic-develops over months.

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Disorders of ineffective red cell production

.
1 Marrow failure
a. Aplastic anemia
 Congenital
 Acquired
b. Pure red cell Aplasia
 Congenital: Diamond– Blackfan syndrome.
 Acquired: TEC
c. Marrow replacement
 Malignancies
 Myelofibrosis
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2. Impaired erythropoietin production
a. Chronic renal disease

b. Hypothyroidism.
c. Chronic inflammation
d. malnutrition
3. Abnormalities of cytoplasmic maturation
a. Iron deficiency
b. Thalassemia syndromes
c. Sideroblastic anemias
d. Lead poisoning

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 
4. Abnormalities of nuclear maturation
a. Vitamin B12 deficiency
b. Folic acid deficiency

5. Primary dyserythropoieitc anemias.

6. Erythropoietic protoporphyria
7. Sideroblastic anemia

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 Disorders of increased red cell destruction or loss
1. Defects of hemoglobin

a. Structural mutants (eg. HbSS, HbSC)
b. Diminished globin production (eg. Thalassemias)
2. Defects of the red cell membrane.
 Hereditary spherocytosis/elliptocytosis/ovalocytosis/stomatocytosis
3. Antibody-mediated.
 Warm /cold /mixed type/drug –induced AIHA

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 .

4. Mechanical injury to the erythrocyte
 Hemolytic uremic syndrome/TTP/DIC

5.Hyperspelinism
6.Bleed loss.

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 II. Morphologic classification

 According to the RBC indices MCV, MCHC.
 MCV –size of RBC.
- may be small (microcytic), normal (normocytic) and large (macrocytic).

 MCHC - value of grams of HGB per 100 mL of RBC.

-Normal(normochromic) is between 32-34 gm/dl.
- lower –hypochromia.higher-hyperchromic

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 HISTORY AND PHYSICAL EXAMINATION 

 Demography (age and sex)


 Neonatal period include recent blood loss, isoimmunization, congenital infection, or
the initial manifestation of a congenital hemolytic anemia
 Iron deficiency anemia
o Before 6 months: Prematurity, neonatal blood loss, maternal anemia.
o School age children: ongoing blood loss, malabsorption, or a very
poor diet.
 X linked disorder –only affects male.

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 
Severity and initiation of symptoms.
Hyperbilirubinemia
Prematurity (Iron, Vitamin E deficiency)
Diet history Type/quantity of milk
Medications
Family history (inherited hemolytic Anemias)
Questions about possible blood loss
Maternal history in the first 6 months.
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 
 Pregnancy/delivery complications
 Pica, nonfood product ingestion.
 Activity level (physical, mental).
 Acute or recent infection.
 Evidence of Endocrinopathy.
 Evidence of liver disease.
 Easy bruising/blood loss.
 History of nematode infestations.
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 Physical examination.
 
Tachycardia suggests an acute process
 Pallor
 A normal heart rate suggests a more chronic process
 Jaundice points to a hemolytic process
 Splenomegaly
 Inherited hemolytic anemia
 Malignancy
 Acute infection
 Hypersplenism
 Petechiae indicate multiple cell lineages are involved.
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 Laboratory
1.First establish anemia Hgb/Hct.

2.Do RBC indices(MCV,MCHC,RDW)
 The lower limit for the MCV(<10 years) approximately 70 fL + age in years
 The upper limit for (>6months) is 84 + 0.6 fL per year until the upper limit of 96 fL.

o Enables classification of anemia

 microcytic
 normocytic or
 macrocytic.
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 
 The red cell volume distribution width (RDW)(SD MCV/mean
MCV)
 reflects the variability in cell size
 used as a measure of Anisocytosis
 The use of the RDW and the total RBC count to aid in further
differentiating between specific etiologies of microcytic,
normocytic, and macrocytic anemia.

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 
3.Asess the white blood cell (WBC) and platelet
counts
 Simple anemia Vs pan/Bicytopenia.
 Elevated WBC and/or platelet count
 most often due to reactive processes
 infection is the most common cause

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4.peripheral morphology

 Assess the size, color, and shape of the red cells
 Macrocytic,Normocytic,Microcytic.
 Central pallor:Excessive(Hypochromia) , Absence (spherocytosis).
 Polychromasia with large cells (reticulocytosis).

 Distinctive abnormalities in shape

 Red cell membrane disorders (eg spherocytosis, stomatocytosis, or
elliptocytosis)
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 Nucleated red blood cells
 Normal only in the newborn

 Indicative of a stressed marrow
 Toxic granulation suggests an acute inflammatory state
 Hyper segmented neutrophils are characteristic of vitamin B12 and Folate
deficiency
 Other investigations (stool, bilrubin, LDH etc)
 Iron studies
 Electrophoresis
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 Physiologic anemia infancy



Normal newborns have higher Hgb than adults
 Within the first week progressive decline in Hgb begins and persist 6-8
weeks
 Hemoglobin-oxygen saturation increases from 50 to 95% or more
 Down regulation of EPO results in decreased erythropoiesis.
 between 8–12 wk of age, hemoglobin concentration reachs 9–11 g/dL.
 The aged RBCs are not replaced as they are normally removed from the
circulation
 Iron from degraded RBCs is stored for future hemoglobin synthesis

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 
 The supply of stored iron is sufficient for hemoglobin synthesis, even in
the absence of dietary iron intake, until approximately 20 wk of age.

 In preterm it is exaggerated and rapid in onset 3-6 weeks, lower Hgb

(7-9gm/dl)

 No therapy is required as it is extra uterine adaptation.

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 Iron deficiency Anemia

 Most common hematologic disease of infancy and childhood.
 More than 30% of world population is suffering from Iron deficiency.
 1mg of iron must be absorbed each day.
 Since only 10% of dietary iron is absorbed a child should have to eat food
containing 10mg of iron.
 Absorption is in the duodenum.
 Term infants develop IDA at 9-24 months.

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 IDA can be caused by;-
o Dietary inadequacy. 
 Delay in introduction of iron rich food
 Feeding of iron poor cow’s milk

o Blood loss- infections such as hookworm.

o Suboptimal store
 In cases of twins and premature babies
o Deficient mother.
o Poor absorption.
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 Clinical manifestations

o

Pallor is the most important sign of iron deficiency.
o Irritability.
o anorexia
o Pagophagia
o Easy fatigability
o Decreased school performance
o Exercise intolerance
o Heart Failure.
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 LABORATORY FINDINGS


 Sequence of biochemical and hematologic events occurring in IDA
are:
 Decrease iron store--- low serum ferritin.
 Serum iron level decreases.
 Iron binding capacity (serum transferrin) increases .
 % saturation (transferrin) decreases.
 As IDA advances RBCS become smaller and HGB decreases
 Low MCV (microcytosis),LOW MCHC( hypochromic )and increased RDW.

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 Treatment

Important diagnostic and therapeutic feature

 Ferrous sulfate 3-6mg/kg of elemental iron in three doses

 should be continued for 8 wk after blood values are normal

 Blood transfusion- if severe Hgb <4gm/dl or if infection or CHF.

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 Therapeutic response

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

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 Prevention
 Women/ pregnant mothers 
 Malaria prophylaxis
 Child spacing
 Know and consume iron rich foods

 During pregnancy and lactation

 Screened for anemia
 Take iron tablets
 Injera, meat and legumes
 Weaning, not long cow’s milk

 Community level
 Educate mothers
 fortification
 Megaloblastic Anemias

o Almost all cases of Megaloblastic anemia's are vitamin
B12 or folate deficiency.

o All are characterized by;

 Ineffective erythropoiesis.
 Macrocytes(high MCV)
 Presence of hypersegemented neutrophils
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 Folic acid deficiency

 Available in green vegetables and animal.
 Absorption is throughout small intestine.
 Body stores are limited and megaloblastic anemia occur 2-3
months after folate free diet.
 Goat milk is deficient in folate.

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 Etiology

 Inadequate intake.
 Decreased folate absorption
 Congenital dihydrofolate deficiency
 Drug induced abnormality (Methotrexate)
 Anticonvulsants decreases absorption.

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 Clinical manifestations

o Peak age 4-7 months
o Irritability
o Failure to gain weight
o Chronic diarrhea

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 Laboratory findings


 MCV –high.
 High LDH
 Hyper segmented neutrophils
 High homocysteine
 Low serum folic acid level(<3 ng/ml)
 Low RBC folate level

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 Treatment

 Folic acid 0.5mg-1mg/day for 3-4 weeks
 Maintenance therapy with multivitamin (0.2 mg
folate)
 Transfusions in severe anemia
 Hematologic response occurs within 72 hrs

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 Vitamin B12 Deficiency

 Mainly animal source.
 After ingestion ,Cobalamin (vit,b12)combines with IF.
 Absorbed in the distal ileum via specific receptors for IF-
cobalamin.
 children's have sufficient vitamin B12 stores to last 3–5 yrs.

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 Etiology

 Inadequate vitamin B12 intake (vegan diet).
 Lack of IF( Hereditary intrinsic factor deficiency)
 Pernicious Anemia
 Impaired vitamin B12 absorption
 Surgery

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 C/M

 Weakness ,irritability and fatigue.
 FTT.
 Pallor
 Glossitis
 Vomiting, diarrhea and icterus
 Neurologic symptoms.

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 Laboratory findings

 High MCV
 Serum vitamin B12 level will be low
 Methylmalonic acid and homocysteine are elevated
 Elevated LDH
 Moderate elevation of serum bilirubin

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 TREATMENT

 Parenteral vitamin B12…duration is based on underlying
cause.
 Reticulocytosis within 2-4 days

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 In summary

 Anemia is a sign of disease and not a final diagnosis.

 The clinician’s goal is to define the underlying cause.

 The anemia may be due to decreased production , increased destruction or loss

of red blood cells.

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 
 Integration of the results of the initial CBC, the peripheral blood smear,
the history and the physical examination can help organize the focus of
further evaluations and, ultimately, minimize the number of tests needed
to make a firm diagnosis.

 In our situation ,always consider the use of cow milk, coexistence of

malnutrition and chronic bacterial infection or parasitic disease like
malaria,hookworm and schistosomiasis.

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 .


Thank you!

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