Childhood Anemia

Dr. Natnael (M.D)

Objectives :

 1-To know what is anemia.

 2-To know different types of anemia.

 3-How to diagnose and treat anemia?

Anemia

Definition :reduction of the red cell volume or

HB concentration below the normal range for
age.

 1- Hemorrhagic Anemia.

 2- Decrease RBCs production.

 3-Hemolytic Anemia.
Classification of anemia
 1-Hemorrhagic anemia.
2-  RBCs production

RBCs precursors Normal RBCs Specific factor

in BM precursors in BM deficiency
(dyshemopoietic)

1-Chronic infection
1- Pure red cell anemia: 1- iron 
2-Chronic
2- B12 
 congenital: Diamond- inflammation
3- Folic A. 
3-CRF
Blackfan syndrome
 acquired: eg.
Autoimmune, viral,
drugs,transient
erythroblastopenia of
childhood
2- Part of pancytopenia:
 Aplastic panccytopenia:
-Congenital: Fanconi a.
-Acquired: 1ry (idiopathic)
2ry (eg. drugs,
Irradiation,
cytotoxic viral
inf, toxins)
3- Hemolytic anemias:

Intracorpuscular causes Extracorpuscular causes

1- Cell wall defect: 1- Immune:

 Heridetary spherocytosis  Isoimmune
 Heridetary elliptocytosis  Autoimmune
 PNH 2- Non-immune:
2-Enzyme defect:  Physical: eg. burn,
 G6PD irradiation
 Pyruvate kinase  Chemical: eg. Drugs, lead,
3- Hemoglobinopathies: snake venom
 Thalassemias  Infection: eg. Malaria,
 Sickle cell anemia clostridium
 Microangiopathies: eg.
DIC, HUS
Symptoms of anemia in children

Non-specific symptoms
--Pallor. –Irritability .
–Poor sleep quality.
–Anorexia.
–Poor concentration and school work.
–Failure to thrive.
•Dizziness / syncope.
•Malaise, easy fatigue, impaired exercise .
tolerance
-Palpitation. - Systolic murmur at base.
-Cardiomegaly. - Congestive HF in
(sever cases).
• Anemia manifesting in neonatal period is
usually result of recent blood loss, iso-immunization,
congenital hemolytic anemia or congenital infection.

• Significant jaundice suggest congenital hemolytic

anemia (e.g. Hereditary spherocytosis, G6PD,
Pyruvate kinase deficiency).

• Nutritional iron deficiency is seldom responsible for

anemia before 6 months of age in term infants
(earlier in preterm infants).
 Thalassemia syndrome more common
in South East Asians and Mediterranean.

 Sickle cell disease more common in Africans.

Diet
 Assess for dietary sources of iron, folic acid and
vitamin B12.
Pica suggest iron deficiency.
 Laboratory
investigations
 CBC
 Haemoglobin : 8.8 g/dl
 Haemotocrite: 32%
 Red cell count:3.100000/cmm
 Red cell indices:

MCV:68.0 fl
MCH:26.3 pg
MCHC: 28.7%
 Leucocytic count: 6100
Basophils: 0%
Esinophils: 2%
Staff : 2%
Segmented:53%
Lymphocytes:41%
Monocytes:2%
 Platelet count :210000 /cmm
The red cell indices in CBC

MCV (mean corpuscular volume)

–The only red cell index directly measured by
the electronic counter.
–Reflects a quantitative defect in the production
of Hb due to ↓hemoglobin synthesis.

– Classify anemia into microcytic, normocytic

and macrocytic types

–Value must be interpreted with age.

•MCHC & MCH are calculate values & therefore
less accurate.

 RDW (Red cell volume distribution width):

–Reflects the variability in cell size and
measures the degree of anisocytosis.
–Normal < 14.5%

–↑ ↑ in Fe deficiency anemia

–Normal in thalassemia trait

Physiological changes in red cell indices
(Hb, Hct, RBC) with age

Very high level at birth

–Relative hypoxemia in fetal life
• Physiological anemia at 2 –3 month of age
–Dramatic reduction in erythropoiesis after birth
–Rapid growth in early infancy
• Gradual rise from childhood to adolescent

• Higher level in male vs female in adulthood

[Effect of androgens vs estrogen,

menstruation].
 Reticulocyte count (RC)
 Reflects the rate at which new RBC are
produced;

Normally < 2% after 3 months; at birth up to

10%.

 Reticulocytosis :in hemolysis and occur as

response to treatment with iron after 48-72h
from start == active BM
 Anemia (Hb and Hct)

MCV, RDW, Retic

MCV

Retic or (N)
RDW(N) Retic, RDW

 Iron deficiency anemia  Thalassemia syndromes

(RDW) (alpha and beta)
 Thalassemia trait
 Lead poisoning Review of smear

 Chronic disease
Further diagnostic test
 Sidroblastic anemia

Review of smear
Hb electrophoresis
Further diagnostic tests

To be continued
 Microcytic anemia
MCV, Retic or (N)

RDW() RDW(N)

Suspect: Suspect:
 Thalassemia trait
Iron deficiency  Lead poisoning
 Chronic disease (inflammation)
 Congenital sidroblastic anemia

Iron therapeutic test

(mild, well, non-sig
hist, correlate with Iron studies (Ferritin,
clinical data) S.iron)

Retics

Serum iron Serum iron N Serum iron Serum iron

Ferritin N or  Ferritin N Ferritin  Ferritin

Anemia of Thalassemia trait Congenital

Iron deficiency
chronic disease sidroblastic
Lead poisoning*
anemia

Hb electrophoresis Bone marrow aspirate

Lead level (sidroblasts)

*Basophilic stippling
in blood film
Causes of iron deficiency anaemia

1-Low birth weight and perinatal hemorrhage.

2-Inadequate dietary iron intake (cow milk ,
↓supplementation).
3-Impaired absorption :chronic diarrhea,
malabsorption, excessive tea, high phytate
intake, antacids, low gastric acidity.
4-Chronic blood loss e.g. cow milk allergy,
peptic ulcer.
 Microcytic anemia (DD)
Get Iron panel: serum iron , TIBC, ferritin

Iron def. dec inc dec

anemia
Siderobla inc dec inc
-stic
anemia
Thalasse inc/nl dec/nl inc/nl
mia -mia
Chronic dec dec inc
disease
Treatment
 Prophylactic :
1-adequate iron to pregnant mother.
2- Breast feeding (exclusive).
3- Iron supplementation after 3rd month, earlier in
premature.

 Curative :
1-ttt cause
2-Oral iron 6mg elemental/kg /day for 3-6m.
3-Parental iron therapy.
4-Packed RBCs in sever cases ---??HF.
 Anemia (Hb and Hct)

MCV, RDW, Retic

MCV (N)

Retic or (N)
RDW(N) Retic, RDW

 Immune hemolysis
 Chronic disease  RBCs membrane disorders
 Transient erythroblastopenia (HS, HE)
of childhood  RBCs enzyme defects
 Acute inflammation (G6PD, PK deficiency)
 Acute hemorrhage  Microangiopathic hemolysis
 Malignancy (HUS, DIC)
 Sickle cell anemia
Review of smear

Further diagnostic tests Further diagnostic tests

 For other  Osmotic fragility

diseases (renal Arranged  Enzyme assays
infection, , liver, according to (G6PD, PK)
metabolic) clinical data  Hb electrophoresis
 Bone marrow  Coomb's test
biopsy

 Anemia (Hb and Hct)

MCV, RDW, Retic

MCV 

Retic or (N)
RDW(N) Retic, RDW

 Folate deficiency  Active hemolysis with brisk

 B12 deficiency
reticulocytosis
 BM failure (aplastic anemia,
Fanconi anemia, DBA)
 Myelodysplastic syndrome
 Hypothyroidism
 Drug induced (anti-convulsants)

Review of smear
Further diagnostic test

Arranged according to clinical data

 Bone marrow aspirate and biopsy

 Folate, B12 level
 Thyroid function test
 Evaluate hemolysis
 Folic acid deficiency anemia

 Asynchrony between nuclear and cytoplasm

maturation→ ↓DNA ,↑RNA → ↑ RBCs size.
 ↓ Serum folate , thrombocytopenia, hemorrahage

 Vit. B12 deficiency (juvenile pernicious

anemia) - tongue smooth ,red, painful.
 Neurological [sensory ataxia, parathesias ,
hyporeflexia, +ve Babiniski, clonus, coma]
 Hemolytic anemias (general features)

 Pallor (acute, chronic) + previous general

features of anemia.

 Tinge of jaundice {indirect hyper-bilirubinaemia}

 Hepato-splenomegaly.

 Stool may be dark.

 Urine (acute crisis →hemoglobinuria)
How to diagnosis?

 Reticulocytosis >2% + nucleated RBCs in

peripheral blood.
 Hyper- bilirubinamia (indirect).
 High serum iron +low iron binding capacity.
 Low RBCs life span.
 low serum Haptoglobin.
 High urobilinogin.
 X-ray : skull, long and short bones, chest and
heart
 Diagnosis of the cause

 Shape of RBCs in blood smear.

 Enzymatic assay.

 Fragility test sickling preparation (Na metabisulfite) .

 Hemoglobin electrophoresis.

 Coombs test.

 Alkaline denaturation test.

 Hereditary Spherocytosis

 AD, abnormal cell membrane.

 Due to abnormal sub-membrane protein skeleton
(Spectrin) → ↑ permeability to Na →spherical
RBCs + ↑ ATP use in Cation pump → premature
aging, especially in spleen → destruction and
chronic hemolysis.
C/P:
 Early onset (jaundice, neonatal anemia).
 Aplastic crisis (Human Parvo-virus).
 Gall bladder stone (pigment stone).
•Splenomegaly ??splenectomy
Investigations :

 All as previous +
 Blood smear
 Osmotic fragility test.

Treatment:
1- Splenectomy ??overwhelming sepsis
[capsulated org.]
2- Blood transfusion
G.6.PD deficiency

 XL- recessive (Glutathione)

 Oxidizing agents or infection.
 Acute hemolysis (abdominal pain, nausea, vomiting,
hemoglobinuria) .
 Anemia ,jaundice.
 Early neonatal presentation.

Diagnosis:
Low Hb, high retic.
Blood smear [Heinz inclusion bodies+ tear drop RBCs].
Enzymatic activity assay(3m).
Treatment

 Prophylactic :
avoid????????

Curative :
1-Mild : observation.
2-Sever: packed RBCS (10-20ml/kg)