ANEMIA IN CHILDREN

kussia[MD]
 Anemia in Children
• Abnormaly low hemoglobin, hematocrit or RBC count, lower
than the age-adjusted reference range for healthy children
• Hemoglobin - a measure of the concentration of the RBC
pigment hemoglobin in whole blood, expressed as grams
per 100 mL (dL)
• Hematocrit (HCT) - the fractional volume of a whole blood
sample occupied by red blood cells (RBCs), expressed as a
percentage
• 1 g/dl Hgb ≈ 3% Hct
• RBC (Red Blood Cells) counted, in millions/mm3
• MCV (Mean Corpuscular Volume):
• Size of average RBC, measured, in femtoliters (fl)
• Lower limit of normal in children:
• 70 + Age (yrs)
• RDW (Red Cell Distribution Width)
• A quantitative measure of the variability of RBC sizes in the
sample (anisocytosis)
• Normal values is 12-14
• Increased in iron deficiency
• MCH(Pg)
• MCHC(g/dl) ..Hgb/Hct
• Reticulocyte Count
• Red blood cell immediately after expulsion of nucleus
• R EFLECTS AMOUNT OF RBC SYNTHESIS
• Reported as percentage, Normal 0.5-1.5%
• Absolute reticulocyte count- %retic x red blood cell
count/L
• Corrected reticulocyte percentage:
• (Actual Hct/expected HCT) X raw retic percentage
• Reticulocyte production index (RPI)= corected
reticulocyte percetage/ RMT( usually 2)
Physiologic classification of anemia
I Impaired red cell formation
A/ Deficiency
• Decreased dietary intake
• Increased demand
• Decreased absorption
• Increased loss
B/ Bone marrow failure
• Failure of a single or all cell lines
• Infiltration
C/Dyshematopoietic anemia
II Blood loss
III Hemolytic anemia
• Corpuscular (membrane, enzymatic or hemoglobine defects)
• Extracorpuscular (immune, idiopathic)
 I. Impaired red cell formation
• A. Deficiency
– Decreased dietary intake (e.g.,
• iron-deficiency
• vitamin B12 , folic acid deficiency
– Increased demand, e.g., growth (iron) hemolysis (folic
acid)
– Decreased absorption
• Specific: intrinsic factor lack- (Vitamin B12)
• Generalized: malabsorption syndrome (e.g., folic acid, iron)
– Increased loss
• Acute: hemorrhage (iron)
• Chronic: gut bleeding (iron)
• Bone marrow failure
– Single cell line
– Two or more cell lines
– Congenital causes
• Fanconi’s anemia
– Acquired causes
• Infections e.g. parvo virus B19
• Malignancies e.g. leukemia, lymphoma,
neuroblastoma…
II. Blood loss
Acute blood loss e.g. hemorrhage due to
trauma, subgaleal hemorrhage, poorly tied
umbilicus…
Chronic blood loss – Hook worm infection, PUD,
Cow’s milk intolerance
Menstrual blood loss in adolescents
III. Hemolytic anemia
A.Corpuscular
1.Membrane defects e.g.spherocytosis
2.Enzymatic defects e.g.pyruvate kinase,G6PD
3.Hemoglobin defects
e.g.Qualitative( sickle cell)
Quantitative( thalasemia)
B.Extra corpuscular
1.Immune – isoimmune
- autoimmune
2.Non immune
Physiologic adjustments to anemia
• Increased cardiac out put
• Increased oxygen extraction
• Increased flow to vital tissues
• Increased 2,3 DPG concentration in RBC “shift
to the right”
• Increased production of erythropoietin(EPO)
 Clinical manifestations
• The clinical manifestations of anemia is the
result of the degree of tissue hypoxia and
etiology of specific cause
• The signs and symptoms of an anemia are a
function of its severity, its rapidity of onset,
and the age of the patient
• In younger individuals, these symptoms and
signs do not appear until the hemoglobin has
fallen below 7-8 g/dL
• With more pronounced anemia, the patient's
exercise capacity can be markedly reduced.
Any exertion is accompanied by palpitations,
dyspnea, a pounding headache, and rapid
exhaustion
• Clinical feature of underlying disease
 Diagnosis
• Anemia is not a specific clinical entity ,is a
manifestation of underlying disease.
• Needs thorough evaluation to reach at
underlying cause.
• Complete evaluation requires thorough
history, physical examination and laboratory
tests.
History
• Patient age ,sex
• Dietary
• drugs
• Blood loss ,jaundice
• Malarial attack , malaria /VL endemicity
• Symptoms of chronic illness
• Family history
• Antenatal ,birth and developmental history
Physical examination
• Pallor (conjunctiva ,mucus membrane
,palm, nail beds ,soles)
• Jaundice ,petechiae /purpura
• LAP ,hepatosplenomegaly
• Evidence of chronic illness
• Anthropometry
Laboratory tests
• CBC
• Peripheral morphology
• Red cell indices
MCV ,MCHC ,MCH
• Red cell distribution width (RDW)
• Reticulocyte count
• Bone marrow aspiration
 Iron deficiency anemia
• Iron deficiency is the most common nutritional
deficiency world wide.
• 30% of global population suffers from iron
deficiency anemia most of whom live in
developing countries.
• Low birth weight infants and adolescents are at
higher risk
• Common in 9-24 month of age
• Iron reclaimed from falling infant hemoglobin
is sufficient for hematopoises in the 1st 6-9
months of life
• 1mg of Fe should be absorbed each day on
average in children.
• Absorption of dietary iron is 10%
• Exclusively breast feed infants require less iron
from other foods
• Increased demand for iron and/or hematopoiesis
–    rapid growth in infancy or adolescence
–    pregnancy
–    erythropoietin therapy
• Increased iron loss
–    chronic blood loss..PUD, early introduction of cows milk ,hook worm
–    menses
–    acute blood loss  
–     polycythemia
• Decreased iron intake or absorption
•    inadequate diet
•    malabsorption from disease
•    malabsorption from surgery
•     chronic inflammation
• Stages:
1) Iron depletion = earliest stage of diminishing iron
stores in the setting of insufficient iron supply
2) Iron deficiency = no anemia, develops as iron
stores are depleted further and begin to impair
hemoglobin synthesis
3) Iron deficiency anemia = supply is insufficient to
maintain normal levels of hemoglobin
 Clinical manifestations
o In mild to moderate iron deficiency no or few symptoms
are noted b/c of compensatory mechanisms.
• Irritability
• Pagophagia/pica
o Moderate to severe iron deficiency
• More prominent irritability ,anorexia
• Pallor ,fatigability ,tachycardia
• High out put murmur
• Cardiac dilatation, poor school performance
Spooning/Koilonichia
 Diagnosis
• History and physical examination
• Hemoglobin
• RBC indices
• Blood smear/peripheral morphology
• Reticulocyte count
• Platelet count
• Serum iron and serum iron binding capacity
(Serum transferin )
• Serum ferritin - decreased
• Stool microscopy
• Differential diagnosis
_Thalasemias
– Lead poisoning
– Sometimes anemia of chronic illness
– Sidroblastic anemia
 Treatment of iron deficiency anemia
• 3-6 mg/kg elemental iron in to three divided
doses
• Duration: 2-3 months after hemoglobin level
and the red cell indices return to normal
• Blood transfusion ( Hgb <4 gm/dl)
Response to iron
 Megaloblastic Anemias
• Anemia with RBC size larger than normal at every
stage of development
• Hyper segmented neutrophils in peripheral smear
• In effective erythropoiesis
• Causes
– Folic acid deficiency
• Inadequate intake
• Decreased absorption
• Congenital folate metabolism defect
• Drug induced folate metabolism abnormalities
– Vitamine B12 deficiency
• Inadequate intake
• Lack of intrinsic factor
• Impaired absorption
• Absence of B12 transport protein
• Both viteB12 and folate are required for the synthesis
of nucleo proteins.
 Clinical manifestation
• weakness, fatigue, failure to thrive, or
irritability
• pallor, glossitis, vomiting, diarrhea
• Neurologic symptoms also occur including
– paresthesias, sensory deficits, hypotonia,
– seizures, developmental delay, developmental
regression, and
– neuropsychiatric changes.
 Laboratory
• RBC indices – increased MCV
• Peripheral morphology – macrocytosis, hyper -
segmented neutrophils
• Reduced serum levels of folic acid/Vitamin
B12
• Neutropenia and thrombocytopenia some
times
• Bone marrow erythroid hyperplasia
• +ve schiling test(vit.B 12)
 Treatment
• Folic acid parentral/oral 0.5-1mg/day x3-4
wks maintain with multivitamin.
• Parentral vit.b12 up to 1mg/day if neurologic
sxs for two weeks ,maintenance every month