ANEMIA IN CHILDREN. In Paediatrics few slides

Anemia in children

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2. ANEMIA IN CHILDREN
Prof Martin NDUWIMANA
KIU 09-09-2022

  
                                     
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3. LEARNING OUTCOMES
•At the end of the lecture and done some
exercises students will be able to:
–Define what is anemia in children
–Discuss the burden of anemia in children
worldwide, in Africa and in Uganda
–Describe the common classifications of anemia
–Determine the causes of anemia
–Establish the diagnosis of anemia
–Determine the criteria of trasnsfusion
–Manage iron deficiency anemia
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4. Definition
•Anaemia is a condition in which the number and size of red
blood cells, or the haemoglobin concentration, falls below
an established cut-off value, consequently impairing the
capacity of the blood to transport oxygen around the body.
•Anaemia is an indicator of both poor nutrition and poor
health.
•In practice, anemia most commonly is defined by
reductions in either hematocrit or hemoglobin or both.
•The threshold for defining anemia is a HCT or HGB
at below -2 SD for: age, sex, race, and location.
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5. Note: normal ranges for HGB
and HCT vary substantially with
age, race, sex and location
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6. L
L
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7. L
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8. Hemoglobin and hematocrit
thresholds for defining anemia
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9. Hemoglobin levels (2 S.D. below mean)
to diagnose anemia in newborns and
infants < 6 months
•Term (cord blood): <13.5 g/dl(mean 16.5 )
•Newborn (1-3 days): <14.5 g/dl (mean
18.5)
•Age 2 weeks: <13.4 g/dl (mean 16.6 g/dl)
•Age 1 month: <10.7 g/dl (mean 13.9 g/dl)
•Age 2-3 months: <9.4 g/dl (mean 11.2 g/dl)
•Age 6 months: <10.5 g/dl (mean 12 g/dl)
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10. Hematocrit: 2 S.D. below mean)to
diagnose anemia in newborns and infants
anemia in infants < 6 months
–Term (cord blood): <42%
–Newborn (1-3 days): <56 %
–Age 2 weeks: <53%
–Age 1 month: <44%
–Age 2-3 months: <35%
–Age 6 months: <36%
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11. Haemoglolobin levels to diagnose anemia in
chidren above 6 months
(WHO)
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12. Epidemiology
•For the year 2019 it is estimated that anemia prevalence in
children aged 6-59 months:
–Global: 40%
–High income countries: 12%
–West and Central Africa: 68%
–East Africa: 53%
–Southern Africa: 43%
•www.thelancet.com/lancetgh Vol 10 May 2022
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13. Epidemiology
•In Uganda(homework):
•Using at least 2 recent references ( 2011-2022), what
is the prevalence of anemia in children in Uganda
–Each student must do the exercise and will share his findings to
his group with a copy to the lecturer(hard copies)
–The group will compile and then synthetize the inputs from the
members and will present the work done before the class with a
copy to the lecturer(hard and soft copies)
–The reports shall indicate the references used
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14. 3. CLASSIFICATION
3 modes of classification:
•
1.Etio-pathophysiological
2.Morphological
3.According to severity level
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15. 1/Etiological classification
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16. 2. Morphologic classification
•Anemia may be classified according to:
–RBC size (mean corpuscular volume, MCV),
–Hemoglobin content (mean corpuscular hemoglobin- MCH), or
–Hemoglobin concentration (mean corpuscular hemoglobin
concentration- MCHC).
•The mean corpuscular volume (MCV) is perhaps the most
useful RBC parameter in the workup of anemia.
–Normal : normocytosis(78-100fL)
–Values may be low: microcytosis( less than 78fL),
–or large:macrocytosis(more than 100fL).
•Microcytic anemia due to iron deficiency is the most common type
of anemia in children.
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17. Reticulocytes count
•An evaluation of the reticulocyte count helps in
defining the etiology of the anemia.-
–Normal ranges of reticulocytes count: 0.8-2.2%
–An increased reticulocyte count is seen as a normal
bone marrow response to ongoing hemolysis or non
chronic blood loss.
–A low reticulocyte count, which reflects decreased
production of red blood cells, is more consistent with
bone marrow depression.
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18. 3/Classification based on level of
severity(WHO)
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19. 4. EVALUATION
•Clinical evaluation
–Thorough history
–Clinical examination
•Paraclinical investigations
–Cells blood count
–Others
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20. Clinical evaluation
•The clinical signs and symptoms of anemia vary
based on the age of the child and the etiology and
chronicity of the anemia.
• Common clinical presentations include the child :
1.the child who is feeling well but is found to have a low
hemoglobin concentration on a routine screening test;
2.the child who is "tired" and does not eat well and a CBC is
asked in the workup context;
3.the child who is being evaluated for other chronic problems
and is found to have a low hemoglobin concentration;
4.the child who is obviously pale, lethargic, and requires
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21. History taking
•The following components should be part of
the history when evaluating an anemic child:
1.Initiation and severity of symptoms
2.Questions relating to hemolytic episodes:
3.History about possible blood loss
4.Questions relating to diet
5.Underlying medical conditions
6.Birth history
7.Family history, race, and ethnicity
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22. Physical examination
•The physical exam will provide important clues as
to the level of severity and to the etiology of the
anemia.
•Check vital signs.
–Patients with acute and severe anemia appear in distress,
with tachycardia, tachypnea, and hypovolemia.
•Patients with chronic anemia are typically well
compensated and usually asymptomatic.
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24. Laboratory evaluation
•The laboratory investigations should begin with a
complete blood count including: red blood cells and its
indices; reticulocyte count; leucocytes; platelets; blood
smear
–These components will allow for morphologic evaluation of the
cells, classification of the anemia based on red blood cell size, and
aid in the identification of the pathophysiologic basis for the
anemia.
•Further investigations will be done according to CBC
results and clinical evaluation findings
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27. 5. TREATMENT
•According to the underlying cause
•Transfusion if severe anemia
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28. Criteria for RBC tansfusion
•Canadian blood services
•https://professionaleducation.blood.ca/en/transfusion/clinical-guide/neonatal-and-pediatric-transfusion
•Published: Wednesday, August 2, 2017
8- 14days
14d- 4mo
0- 7 days
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29. Criteria for RBC tansfusion
•Canadian blood services
•https://professionaleducation.blood.ca/en/transfusion/clinical-guide/neonatal-and-pediatric-transfusion
•Published: Wednesday, August 2, 2017
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30. Amount of blood transfusion
10-20ml/kg of red cells
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31. IRON DEFICIENCY ANEMIA
(IDA)
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32. Learning outcomes
At the end of the lecture you will be able to:
Describe the burden of IDA
Determine the causes & consequences of IDA
Diagnose IDA
Describe the strategies for control & prevention
of IDA
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33. IDA definition
•IDA is a state in which there is
insufficient iron to maintain the
normal physiological function of
blood and tissues, such as the brain
and muscles.
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34. IDA definition
•Iron deficiency may develop in the absence
of anemia and the tissues may be affected
from this condition.
•Iron deficiency develops in three stages.
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35. Stages of ID
•1. Prelatent stage:
–There is reduction or absence of bone marrow iron stores and reduced
serum ferritin level.
–Serum iron concentration, hemoglobin and hematocrit are normal.
•2. Latent stage:
–Serum iron (SI) and trasferrin saturation are reduced in addition to
reduced iron stores.
–Hb and Hte are within normal limits.
•3. Marked IDA:
–Hemoglobulin and hematocrit levels are reduced.
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36. IDA EPIDEMIOLOGY
Iron deficiency is the most common
micronutrient deficiency in the world
affecting 1.3 billion people i.e. 24% of the
world population.
–In comparison only 275 million are iodine
deficient and 45 million children below age 5
years are Vitamin A deficient.
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37. PREVALENCE OF ID
Region 0-4yr 5-12yr

Africa 56% 49%

Developed12% 7%
World 43% 37%

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38. IRON METABOLISM
•Sources of iron
•Absorption see biomedical level
•Transport
•
•Storage
•Role
•Consequences of ID
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39. Storage of iron
Tissues with higher requirement for iron
( bone marrow, liver & placenta) contain more
transferrin receptors.
Once in tissues, iron is stored as ferritin &
hemosiderin compounds, which are present in the
liver, RE cells & bone marrow.
The amount of iron in the storage compartment
depends on iron balance (positive or negative).
Ferritin level reflects amount of stored iron in the body
& is important in assessing ID.
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40. Role of iron
Iron have several vital functions:
•Formulation of hemoglobin
•Binding O
2 to RBC and transport
•Transport of electrons within cells
•Co-factor of essential enzymatic reactions:
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41. Role of iron
Co-factor of essential enzymatic reactions:
Neurotransmission
Synthesis of steroid hormones
Synthesis of bile salts
Detoxification processes in the liver
Regulation of Body temperature
Muscle activity
Catacholamines metabolism
Immune system – T cell antibodies
Brain Dev & function
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42. Consequences of ID
 OnOn physical growth and performancephysical growth and performance
•Impaired wweight gain, growth velocity
•Poor work capacityPoor work capacity
• Decreased endurance, work capability
•T cell and antibodies decrease
•Cell mediated immunity defective
•Poor killing bacteria capabilities
•Poor capacity of leucocyte defense
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43. Consequences of ID
 On mental and psychomotor developmentOn mental and psychomotor development
•Poor attentiveness
• Poor memory
•Poor academic performance on vocabulary,
reading , writing, arithmetic
• Disruptive, irritable, restlessness
• Poor performance in tests
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44. AGE RELATED RISKS
GROUPS
•0- 24 months: age group at the highest risk
for ID,
–Rapid growth + inadequate intake of dietary
iron.
–In full-term infants, the iron stores can meet the
iron requirements until ages 4-6 months, and
IDA generally does not occur until
approximately 9 months of age.
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45. AGE RELATED RISKS
GROUPS
•Preterm and low-birth-weight infants are
born with lower iron stores and grow faster
during infancy.
–Consequently, their iron stores are often
depleted by two to three months of age and they
are at greater risk for IDA
•
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46. AGE RELATED RISKS
GROUPS
•After 24 months of age, the growth rate of children
slows and the diet becomes more diversified, the risk
for IDA drops.
•After 36 months of age, dietary iron and iron status
are usually adequate;
–However , risks for IDA include limited access to food, a
low-iron or other specialized diet, and medical conditions
that affect iron status (e.g., malaria and/or parasitic
infections)
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47. ETIOLOGY
Inadequate intake of iron & of food which
enhances iron absorption.
High intake of inhibitors of iron absorption
Hookworm infestation.
Blood loss (heavy menses & use of aspirin
& NSAID).
Low iron stores in newborns.
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48. DIAGNOSIS OF IDA
Clinical: symptoms (fatigue, dizziness ,
palpitations..etc) & signs (pallor, smooth
tongue, Koilonychia, splenomegaly &
dysphagia in elderly women).
Laboratory
Stainable iron in bone marrow
Response to iron treatment
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49. Clinical manifestations
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50. Lab findings
Microcytic hypochromic anaemia
–Low Hb level (< 11.0 g/dl)
Low MCV, MCH, MCHC
Low serum iron < 40μg/dL)
Low serum ferritin(<10 μg/L): test together with CRP
High Total iron-binding capacity (N:240–450 μg/dL)
Low transferrin saturation(< 15%)
Reticulocyte hemoglobin content(< 26 pg/cell)
Increased serum transferrin receptor 1 (TfR1).
Increased serum Zn erythrocyte protoporphyrin
Increased serum Free erythrocyte protoporphyrin
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51. TREATMENT
Blood transfusion if heart failure is
eminent
Oral iron 3-5 mg Fe/kg/day
Treat underlying cause
Dietary education
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52. Treatment
•Goal : to replace iron stores, not just circulating
Hgb!
•Oral iron supplementation:
– 3 - 6mg/kg/day of elemental iron
•Results:
–Subjective improvement in CNS: 24-48hr
–Reticulocytes- starts to rise in 3 -4 days,
–Hbg/Hct- after 4- 5 days (Hb of 0.25-0.4 g/dl per
day or 1%/day rise in hematocrit)
•After Hgb normalisation : continue Fe therapy
1-2 months to replace Fe stores
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53. Oral iron formulations and dosing
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54. Treatment
•Parenteral iron treatment can be
administered when:
– oral iron treatment can not be tolerated,
–anemia should be corrected rapidly
–Gastrointestinal absorption disorders including
celiac disease or inflammatory bowel disease.
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55. Prevention
•Primary prevention:
–Delayed umbilical cord clamping
•approximately 120 to 180 seconds after delivery
–Dietary interventions: breastfeeding and
fortification of formula (if not breast-fed) or
infant cereal.
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56. PREVENTION
•Primary prevention(contd):
–Supplementation:
•Healthy exclusively breast-fed infants:
–1 mg/kg/day of oral iron beginning at four months of age until
iron-containing complementary foods are introduced.
–Whole milk should not be introduced before 12 months of age.
–Red meat and vegetables with higher iron content should be
introduced early.
•Preterm & SGA infants breastfed :
–2 mg/kg/day of iron supplement by one month of age until
weaned to iron-fortified formula or beginning complementary
foods.
•Secondary prevention:
•identify children with IDA through screening programs.
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57.  Iron deficiency is major public health problem
 It is an essential nutrition not only for normal growth
health and survival of children but also for their mental and
cognitive development.
•Iron deficiency anemia is associated with significantly
poorer performance on psychomotar and mental
development scale and behavioral rating in infants and
children.
Iron supplementation improves mental development
score modestly and improve physical capacity and
endurance.
CONCLUSION
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